Medical

Emergencies
Guidebook

Editors:

Prof. Hasan Abu Aisha

Dr. Elwaleed Ali Mohamed
 Medical Emergencies
Guidebook
Editors:

Hasan Abu Aisha, FRCP (Chief Editor),

Professor of Medicine and Nephrology, President of National Ribat University
Elwaleed Ali Mohamed Elhassan, MRCP, ABIM
Assistant Professor of Medicine,Faculty of Medicine,University of Khartoum
Researcher, National Ribat University Academic office

Section-Editors:

A. E. Abdelghani, MRCPsych, DPM, DCP,

Assistant Professor of Psychiatry Consultant Psychiatrist, National Ribat
University
Ahmed Ali Ahmed Suliman, MACP, ABIM,
Internist & Cardiologist Sudan Heart Center
Ala’Eldin Hassan Ahmed, MD, FRCP, FCCP
Associate Professor of Medicine, Consultant Physician and Pulmonologist
MoH
Amira Abbas Mohamed Fadl, FRCP Assistant Professor of
Medicine,Consultant Physician and Gastroenterologist, National Ribat
University
Elwaleed Ali Mohamed Elhassan, MACP, ABIM
Hisham Abdel Rahim, FRCP,Assistant Professor of Medicine,
Consultant Physician and Endocrinologist National Ribat University
 Contributors
Neurology:

 Prof. Dawod Mustafa

 Dr. Hassb El Rasoul Siddig Ali

 Dr. Mohamed Najeeb

 Dr. Ammar El Tahir

 Dr. Abashar Hussian

Cardiology:

 Prof. Siddig

 Dr. Nawal El Kordofani

 Dr. Mohamed Saeed AL Khalifa

 Dr. Ahmed Babiker

 Dr. Adel El Boshi

Gastroenterology and Infectious diseases :

 Prof. Salih Yassin

 Prof. Suliman Salih Fudial

 Prof. Mohamed Siddig Ali

 Dr. Abdul Gadir El Kadro

 Dr. Fatima Farah

 Dr. Huda El bagir

 Dr. Baha El din Gasm El seed

 Dr. Hatim Modawi

 Dr. Mohamed El Tahir

Nephrology and Poisoning :

 Prof. Abdul Rahman Ali

 Dr. Salma Suliman

  Dr. Gahelnabi

Respiratory diseases :

 Dr. Abdul lateef Gasem alla

 Dr. Mohamed EL bagir

Endocrinology :

 Prof . Mahadi Mohamed Ali

 Dr. Ali El Zayyat

Psychiatric diseases :

 Prof. Abdul-Aal El idrisi

Coordinated by:

 Dr. Amir Elssoni Mahjoub

 Dr. Ayat Hussin Halfawi

 Table of Contents
Editors:.............................................................................................................................................................2
Contributors......................................................................................................................................................3
Preface............................................................................................................................................................10
Acknowledgment...........................................................................................................................................11
Foreword........................................................................................................................................................12
Approach to Common Emergency Symptoms..........................................................................................................
Chest Pain...........................................................................................................................................................15
Differenial diagnosis......................................................................................................................................15
Acute Fever........................................................................................................................................................17
Definition:......................................................................................................................................................17
Diagnostic Approach:.....................................................................................................................................17
Pertinent Investigations:.................................................................................................................................17
Management:..................................................................................................................................................18
Table of drugs used in this section:................................................................................................................21
Approach to Headache in the Emergency Department (1)................................................................................22
Approach to Medical Causes of Acute Abdominal Pain....................................................................................25
Introduction:...................................................................................................................................................25
Causes:...........................................................................................................................................................25
Investigations:................................................................................................................................................26
Management:..................................................................................................................................................26
Various General Medical Emergencies..................................................................................................................27
Shock..................................................................................................................................................................28
Hypovolemic Shock.......................................................................................................................................28
Distributive Shock..........................................................................................................................................29
Drugs used in this section:.............................................................................................................................31
Coma..................................................................................................................................................................32
Definition:......................................................................................................................................................32
Causes:...........................................................................................................................................................32
Management:..................................................................................................................................................32
Approach to Drug Overdose and Poisoning.......................................................................................................34
Cardiovascular Emergencies..................................................................................................................................38
Acute Coronary Syndromes...............................................................................................................................39
Evaluation of patients with suspected ACS:..................................................................................................39
Management:..................................................................................................................................................40
Management specific to ST Elevation myocardial infarction:.......................................................................40
Management specific for Unstable Angina/Non-ST elevation myocardial infarction(UA/NSTEMI)..........41
Acute Cardiogenic Pulmonary Edema...............................................................................................................42
Definition:......................................................................................................................................................42
Diagnosis and clinical evaluation:..................................................................................................................42
Investigations:................................................................................................................................................42
Treatment:......................................................................................................................................................43
Additional therapy:.........................................................................................................................................43
Cardiogenic Shock.............................................................................................................................................45
Definition.......................................................................................................................................................45
Management...................................................................................................................................................45
Drugs used in this section:.............................................................................................................................46
Endocrine Emergencies..........................................................................................................................................48
Diabetic Ketoacidosis (DKA)............................................................................................................................49
Essentials of diagnosis:..................................................................................................................................49
Differential diagnosis:....................................................................................................................................49
Clinical Presentation......................................................................................................................................49
Precipitating factors:......................................................................................................................................49
Diagnostic studies:.........................................................................................................................................49
Treatment:......................................................................................................................................................49
Features of resolution of DKA:......................................................................................................................50
Complications of treatment:...........................................................................................................................51
 Notes..............................................................................................................................................................51
Hyperosmolar Nonketotic Coma........................................................................................................................52
Definition.......................................................................................................................................................52
Essentials for diagnosis:.................................................................................................................................52
Differential diagnosis:....................................................................................................................................52
Precipitating factor:........................................................................................................................................52
Clinical Presentation......................................................................................................................................52
Diagnostic studies:.........................................................................................................................................53
Goals of treatment:.........................................................................................................................................53
Treatment:......................................................................................................................................................53
Complications of treatment:...........................................................................................................................54
Diabetic Lactic Acidosis....................................................................................................................................55
Management:..................................................................................................................................................55
Correction of acidosis:...................................................................................................................................55
Hypoglycemia....................................................................................................................................................56
Definition:......................................................................................................................................................56
Common Precipitants:....................................................................................................................................56
Clinical Presentation:.....................................................................................................................................56
Management:..................................................................................................................................................56
Thyroid Storm....................................................................................................................................................57
Definition:......................................................................................................................................................57
Clinical Manifestations:.................................................................................................................................57
Management:..................................................................................................................................................57
Addisonian Crisis...............................................................................................................................................58
Diagnosis:.......................................................................................................................................................58
Management:..................................................................................................................................................58
Pituitary Apoplexy.............................................................................................................................................59
Diagnosis:.......................................................................................................................................................59
Management:..................................................................................................................................................59
Myxedema Coma...............................................................................................................................................59
Management...................................................................................................................................................59
Gastro-intestinal Emergencies................................................................................................................................60
Acute Diarrhea In Adults...................................................................................................................................61
Definition:......................................................................................................................................................61
Pathogenesis:..................................................................................................................................................61
Causes............................................................................................................................................................61
The transport vehicle of the common classic pathogens................................................................................61
Clinical Assessment:......................................................................................................................................62
Possible risk factors for infectious diarrhea:..................................................................................................62
Investigations:................................................................................................................................................62
Management:..................................................................................................................................................62
Recommended Antimicrobial therapy...........................................................................................................63
Diarrhea workup algorithm: (Diarrhea < 3 weeks duration ).......................................................................64
Upper GIT Hemorrhage.....................................................................................................................................65
Introduction:...................................................................................................................................................65
Definitions :....................................................................................................................................................65
Etiology:.........................................................................................................................................................65
Admission arrangements:...............................................................................................................................65
Blood tests taken urgently at initial presentation...........................................................................................65
Assessment of bleeding severity:...................................................................................................................66
Management:..................................................................................................................................................67
Allgorithm for the management of acute gastrointestinal hemoarrhage........................................................69
Treatment of Bleeding Esophageal Varices.......................................................................................................70
Definitions:.....................................................................................................................................................70
Pathogenesis:..................................................................................................................................................70
Mortality /Morbidity:.....................................................................................................................................70
Common Causes of Portal Hypertension:......................................................................................................70
Differential diagnosis:....................................................................................................................................71
Treatment approaches:...................................................................................................................................71
 Drugs used in this section..............................................................................................................................75
Table 1. Child-Pugh classification of cirrhosis..............................................................................................75
Bleeding esophageal varices..............................................................................................................................77
Lower Gastrointestinal Bleeding........................................................................................................................78
Definition:......................................................................................................................................................78
Causes:...........................................................................................................................................................78
Management:..................................................................................................................................................78
Hepatic Encephalopathy and Fulminant Hepatic Failure (FHF)........................................................................79
Definitions:.....................................................................................................................................................79
Pathogenesis:..................................................................................................................................................79
Causes of Fulminant Hepatic Failure.............................................................................................................79
Diagnosis and investigation of FHF:..............................................................................................................80
Prognosis:.......................................................................................................................................................80
Management of FHF:.....................................................................................................................................81
Clinical Features of Hepatic Encephalopathy:...............................................................................................82
Common Precipitants of Hepatic Encephalopathy in Liver Cirrhosis...........................................................82
Differential Diagnosis for Hepatic Encephalopathy......................................................................................83
Management of Hepatic Encephalopathy......................................................................................................83
Drugs used in this section..............................................................................................................................86
Respiratory Emergencies........................................................................................................................................87
Management of Acute Asthma Exacerbations in Adults...................................................................................88
Definition:......................................................................................................................................................88
Differential diagnosis:....................................................................................................................................88
Directed Approach to Acute Asthma Exacerbations:....................................................................................88
Drugs used in this section:.............................................................................................................................90
Algorithm of Management of Acute exacerpation of athma in adult in emergency department...................91
Spontaneous pneumothorax...............................................................................................................................92
Definition:......................................................................................................................................................92
Differential diagnosis:....................................................................................................................................92
Directed Approach to spontaneous pneumothorax:.......................................................................................92
History:...........................................................................................................................................................92
Physical examination:....................................................................................................................................92
Diagnostic studies:.........................................................................................................................................92
Recommended algorithm for the treatment of primary spontaneous pneumothorax.....................................94
Recommended algorithm for the treatment of spontaneous secondary pneumothorax.................................95
Management of Acute Pulmonary Embolism....................................................................................................96
Differential diagnosis:....................................................................................................................................96
Directed Approach to Acute Pulmonary Embolism:......................................................................................96
Drug treatment of acute pulmonary embolism...............................................................................................97
Rules for predicting the probability of embolism..........................................................................................98
Renal, Hypertensive and Electrolyte Emergencies..............................................................................................101
Acute Renal Failure..........................................................................................................................................102
Definition:....................................................................................................................................................102
Etiology:.......................................................................................................................................................102
Clinical presentation:....................................................................................................................................103
Workup:........................................................................................................................................................103
Treatment:....................................................................................................................................................104
Drugs used in this section:...........................................................................................................................105
Hypertensive Crises.........................................................................................................................................106
Definition:....................................................................................................................................................106
Hypertensive Emergency.............................................................................................................................106
Hypertensive Urgency..................................................................................................................................108
Drugs used in this section:...........................................................................................................................111
Hypokalemia....................................................................................................................................................112
Definition:....................................................................................................................................................112
Etiology:.......................................................................................................................................................112
Presentation:.................................................................................................................................................112
Workup:........................................................................................................................................................112
Management:................................................................................................................................................113
 Hyperkalemia...................................................................................................................................................114
Definition:....................................................................................................................................................114
Etiology:.......................................................................................................................................................114
Presentation:.................................................................................................................................................114
Workup:........................................................................................................................................................114
Treatment:....................................................................................................................................................115
Emergent Treatment of Hyperkalemia.........................................................................................................117
Non-emergent Treatment of Hyperkalemia.................................................................................................117
Hyponatremia...................................................................................................................................................118
Definition:....................................................................................................................................................118
Workup:........................................................................................................................................................118
Hypotonic Hyponatremia:............................................................................................................................118
Drugs used in this section:...........................................................................................................................119
Hyponatremia algorithm..............................................................................................................................120
Hypernatremia..................................................................................................................................................121
Definition:....................................................................................................................................................121
Workup:........................................................................................................................................................121
Treatment:....................................................................................................................................................121
Drug used in this section:.............................................................................................................................124
Hypercalcemia..................................................................................................................................................125
Definition:....................................................................................................................................................125
Clinical Presentation:...................................................................................................................................125
Workup:........................................................................................................................................................125
Best Practice Treatment Algorithm:.............................................................................................................125
Causes of Hypercalcemia:............................................................................................................................126
Drugs used in treatment of hypercalcemia:..................................................................................................129
Neurologic Emergencies......................................................................................................................................130
Stroke (Cerebrovascualr Accident)..................................................................................................................131
Definition:....................................................................................................................................................131
Management Steps:......................................................................................................................................131
Table of drugs used in this section:..............................................................................................................135
Status Epilepticus.............................................................................................................................................137
Definition:....................................................................................................................................................137
Predisposing factors:....................................................................................................................................137
Management Steps.......................................................................................................................................137
Table of drugs used in this section:..............................................................................................................142
Psychiatric Emergencies......................................................................................................................................143
Psychiatric Emergencies..................................................................................................................................144
Management of aggressive violent patients.....................................................................................................144
Introduction..................................................................................................................................................144
Definitions....................................................................................................................................................144
Presentation..................................................................................................................................................144
Differential diagnosis...................................................................................................................................145
Assessment / work-up..................................................................................................................................145
Investigations...............................................................................................................................................146
Management.................................................................................................................................................146
Important notes:............................................................................................................................................148
The suicidal Patient..........................................................................................................................................150
Definitions....................................................................................................................................................150
Presentation..................................................................................................................................................150
Differential Diagnosis..................................................................................................................................150
Management.................................................................................................................................................150
The unresponsive patient (Stupor)..................................................................................................................152
Definition.....................................................................................................................................................152
Presentation..................................................................................................................................................152
Differential diagnosis...................................................................................................................................152
Management: see chart................................................................................................................................152
Neuroleptic malignant syndrome (NMS)........................................................................................................154
Definition.....................................................................................................................................................154
 Presentation..................................................................................................................................................154
Laboratory abnormalities.............................................................................................................................154
Differential diagnosis...................................................................................................................................154
Management: see chart...............................................................................................................................154
Other neuroleptic-induced problems................................................................................................................155
Other neuroleptic-induced problems................................................................................................................156
Acute dystonias............................................................................................................................................156
Akathisia (restlessness)................................................................................................................................156
Drugs used in psychiatric emergencies........................................................................................................156
Appendix 1.......................................................................................................................................................157
Malaria.........................................................................................................................................................157
Appendix 2.......................................................................................................................................................158
List of Abbreviations Used in This Guidebook...........................................................................................158
Appendix 3.......................................................................................................................................................161
Table of Drugs Used in This Guidebook.....................................................................................................161
 ‫‪Preface‬‬
‫بسم هللا الرحمن الرحيم‬
‫الحمد هلل ربِّ العالمين حمداً كثيراً طيِّب ا ً مُبارك ا ً في ه كم ا يُحبُّ ربُّن ا ويرض ى‪ ،‬وص لى هللا‬
‫وسلَّم وبارك على عبده ورسوله نبيِّنا مُحمَّد إمام المُرسلين وسيِّد الدعاة وعلى آله وصحبه ومن‬
‫بإحسان إلى يوم الدين ‪ ،‬وبعد ‪،‬‬
‫ٍ‬ ‫تبعهم‬
‫فيُسعِد ُني أن أُق ِّدم ألبنائي وإخواني األطِ ب اء ه ذا ال دليل ال ذي يَعت ني بتوف ير ال ُّنص ح الس َّديد‬
‫والحرجة ‪ .‬وق د ب ذل بعض األس اتِذة األ ِجالء‬ ‫الطارئة‬ ‫للتعامُلِ مع مرضى حاالت ِّ‬
‫الطب الباطِ ن‬
‫ِ‬ ‫ِ‬
‫جهداً مُق َّدراً في تأليف أصل هذا الكِتاب ‪ُ ،‬ث َّم يسَّر هللا ع َّز وج َّل ُثلَّة من ُزمالئهم ق اموا بتنقيح ه‬
‫وصوغ ُه وترتيب ما َّدته على نحوٍّ نسأ ُل هللا أن يُرضي به القُرَّ اء وينفع به إخواننا األطِ باء ‪ .‬وق د‬
‫َّ‬
‫توخت لجنة إعداد الكِتاب أن تجمع بين فضيلتين وهما إيراد الطريقة المُثلى للعالج مع ذِكر م ا‬
‫تيسَّر من البدائِل المُتاحة محليا ً ‪.‬‬
‫وإ َّننا إذ ُنق ِّدم هذا الدليل إلخوانن ا األطِ ب اء ل نرجو أن يك ون مُعين ا ً لهم على أداء عملهم على‬
‫كال التوض يحية م ع ذِك ر‬ ‫خير وجه ‪ ،‬و َمعينا ً يس تقون من ه المعلوم ة الم َّ‬
‫ُيس رة والمُدعَّم ة باألش ِ‬ ‫ِ‬
‫فهرس للعقارات الرئيسة في خاتِم ِة ُك ِّل فصل ‪.‬‬
‫ٍ‬
‫هذا ونسأ ُل هللا َّ‬
‫عز وج َّل أن يُكتب له ذا ال دليل القب ول في الس ما ِء واألرض ‪ ،‬وأن ينف ع ب ه‬
‫البالد والعباد ‪ ،‬وأن يكتبه في صحائِف أعمالنا جميعا ً وأن يُجزي المس ئولين في وزارة َّ‬
‫الص حة‬
‫خير الجزاء لتفضُّلها بنش ر ه ذا ال دليل وإعتم ادهِ ‪ .‬ولمَّا ك ان ُك ل جه د بش ري مُعرَّ ض ا ً للزل ل‬
‫والخط أ ‪ ،‬فإنن ا نطلُب من إخوانن ا األس اتِذة العُلم اء أن ال يبخل وا علين ا بنص ائِحهم الس ديدة‬
‫وتوجيهاتهم الرشيدة حتى ينفع هللا بهذا الدليل ‪.‬‬
‫األُستاذ الدكتور ‪ /‬حسن أبو عائِشة‬
‫رئيس المُحرِّرين‬
 Acknowledgment

The unique purpose of this effort, which is represented in the

development of The Management Protocol for Medical Emergencies
(Medical Emergency Guideboock), is to ensure that the best available
knowledge concerning the use of Quality programs to improve health
outcome is properly used.
I greatly appreciate the hard efforts that have been put into this
work. My sincere gratitude and appreciation goes to the contributors
who drafted this protocol and to all members of the Sudanese
Physicians Association, and Ribat National University whose
response has provided valuable insight and guidance in endorsement
of this document.
My thanks and great appreciation is extended to Professor
Hassan Aboasha and Dr Alwaleed Ali, the editors, who dedicated a
lot of their precious time to edit this Protocol; and to Professor El
Rashid Ahmed Abdullah, Chairman of the Management Protocol for
Emergencies Committee, who gave invaluable assistance throughout
the whole work.
We hope that the "Medical Emergency Guideboock", will be
valuable in continuous medical professional education and
improvement of Medical care to achieve our ultimate goal by
reducing their morbidity and mortality rates.

Dr Abdullah Sid Ahmed Osman,

Undersecretary, Federal Ministry of Health
 Foreword
Over the last decades, there has been a growing concern for the
Quality issue, particularly in the developing countries. The principles
of quality management have become indispensable in the
comprehensive efforts being carried out to improve health services.
Quality Improvement has always been a major focus of the
Federal Ministry of Health (FMoH). To this effect, the FMoH has
taken the role of leadership in various efforts to upgrade the quality of
health services.
Quality program in health services is new to Sudan; it had been
established in September 2001. The program aims to consistently
provide a service that meets customer and applicable regulatory
requirements by introducing Total Quality management in healthcare
organizations in primary, secondary and tertiary levels. The Quality
directorate started to implement many programs that increased
efficiency and capabilities of health organizations.
First of the entire process, Quality directorate has established
Quality Programs in certain hospitals as a pilot projects, then it will be
expanded to other health organizations all over the country. Many
achievements took place since its establishment: awareness had been
increased among health workers in different healthcare organizations;
most of the basic required documents has been developed and
endorsed; Triage system has been implemented in one example
hospital, Khartoum North Teaching Hospital, and now spreads to
Khartoum and Omdurman Teaching Hospitals. Patients' and
employees' satisfaction and patients' complaint programs have been
implemented, National Infection Control Program has been
established and Internal Auditing has been applied.
Management protocols for emergencies are achievements of
successful partnership between the FMoH and Sudanese associations
of specialists in different disciplines. This effort aims to achieve
continuous medical professional education, most appropriate and up-
to-date medical care and low morbidity and mortality rates.
 We are looking forward to see these Protocols of use to our
young doctors throughout the country and to realization of the above
mentioned purposes.

Dr Malik Abdo Ali,

MSc, MD, Consultant Community Medicine,
Director General, Quality Directorate, FMOH
 Approach to Common
Emergency Symptoms
 Chest pain

 Acute fever

 Headache

 Acute abdominal pain

 Chest Pain
Editor: Ahmed Ali Ahmed Suliman

Chest pain is a frequent complaint with a wide differential diagnosis. The aim of evaluation
in an emergency room is to exclude or identify life threatening conditions and provide
emergency treatment.
Any patient presenting with prolonged chest pain >10 min should have a focused history and
examination as well as an ECG. Chest X-ray is obtained if seen necessary.
The emergency room physician should specifically look for the following serious conditions
which may present with chest pain:

Differenial diagnosis
1- Acute ST elevation myocardial infarction- (Presumed) New ST elevation or LBBB on
ECG with prolonged chest pain.
2- Unstable angina/Non ST elevation myocardial infarction-prolonged chest pain with
significant ST depression or deep T wave inversion. N.B. ECG may be normal.
Therefore patients with strong clinical suspicion (multiple coronary artery risk factors,
typical chest pain) with normal or non-diagnostic ECG should be considered as
suspected ACS (acute coronary syndrome) till serial ECGs and cardiac markers are
negative. Please refer back to ACS section for more details.
3- Aortic dissection. Classically there is acute severe persistent chest pain that radiates to
the back often in patient with history of hypertension or Marfan’s syndrome. Pulses
may be unequal and mediastinum may be wide on chest X-ray.
4- Pulmonary embolism. Sudden onset of shortness of breath accompanied by central
chest tightness or pleuritic type chest pain in a patient at risk for deep venous
thrombosis(postoperative, prolonged bed rest, prior venous thrombosis, etc.) .Look for
evidence of DVT.
5- Pneumothorax. This may be spontaneous or secondary in patients with lung disease
e.g. during acute asthma or in patients with TB. There is acute shortness of breath
with pleuritic pain to the lateral side of the chest wall with physical signs of
pneumothorax- hyper-resonance with absent breath sounds.
6- Boerrhave’s syndrome. This acute mediastinitis from esophageal rupture. Central
chest pain following prolonged vomiting usually with circulatory collapse. There vis
may be associated hydropneumothorax. Confirm with barium swallow. Immediate
surgical referral.

There are other many causes like esophageal reflux, pericarditis, musculoskeletal pain.etc. .
Patients with low risk for coronary artery disease or pulmonary embolism, with atypical chest
pain (e.g. ill defined chest pain to the sides, or pain exacerbated by movement suggesting
muscular pain, sharp short lived pain..etc.) who have normal examination, ECG and CXR and
life threatening situations excluded , can be given symptomatic treatment(e.g. NSAID or
antacids) and investigated on an outpatient basis.
 Chest Pain

Obtain history and

examination
ECG
CXR

Definite or suspected Low risk

Acute Coronary Aortic Dissection IF symptoms are patients with
Syndrome. suspected. predominantly atypical
ECG shows ST Severe pain radiates pulmonary i.e. symptoms,
elevation or to the back, unequal shortness of breath normal exam
depression, LBBB, pulses, wide medias- or pain is pleuritic and ECG and
deep T inversions or tinum on CXR life-threat-
ECG nondiagnostic ening
but strong clinical conditions
suspicion excluded

-Control BP: IV Exclude

nitroprusside or pneumothorax
nitrates by exam and
-If not available use CXR Symptomatic
Refer to ACS ACE-I treatment
section -B blockers to Outpatient
control heart rate follow-up
-Avoid aspirin and If pulmonary
anticoagulants. embolism is
- Seek to confirm suspected
dissection by CT+,
MRI, Trans-
esophageal echo, or
aortography. -IV unfractionated heparin (or
low molecular weight heparin)
-Seek to confirm with V/Q scan,
CT angiogram, pulmonary
angiogram or lower extremity
Doppler.
 Acute Fever
Editor: Elwaleed Ali Mohamed Elhassan

Definition:
Acute fever is defined as fever lasting for 7 days or less.
Common causes of acute fever include:
 Malaria
 Respiratory infections:
o Upper respiratory tract infections (URTI): tonsillitis, pharyngitis, otitis media, sinusitis.
o Lower respiratory tract infections (LRTI): pneumonia, bronchitis.
 Abdominal infections:
o Intestinal: enteric fever, dysentery and colitis
o Acute viral hepatitis.
o Liver abscess (amoebic or pyogenic )
o Biliary infections: eg cholecytisis, ascending cholangitis
 Urinary tract infections
 Nervous system infections: meningitis, encephalitis
 Skin: impetigo, erysipelas, cellulitis and abscesses.
 Musculoskeletal system: septic arthritis and acute osteomyelitis.

Diagnostic Approach:
Confirm the high temperature. Check the vital signs. Examine thoroughly for associated
signs: neck, throat, skin rash, lymph nodes, chest, liver and spleen.
The following combinations are helpful diagnostic clues:
 Fever + headache + arthralgia + vomiting malaria.
 Fever + sneezing + cough + runny nose upper respiratory tract infection.
 Fever + burning micturition, loin or suprapubic pain UTI.
 Fever + upper abdominal pain and tender mass hepatitis, liver abscess or
cholecystitis.
 Fever + coma cerebral malaria or encephalitis.
 Fever + headache + neck stiffness meningitis or encephalitis.

Pertinent Investigations:
The following investigations may be performed selectively as dictated by clinical
impressions:
 Total white blood cell count (TWBC):
o High count with neutrophil predominance and presence of band cells suggests
pyogenic infections e.g., pneumonia, tonsillitis. pyogenic liver abscess (etc)
 Blood film for malaria (a Giemsa-stained thick and/or thin blood smear for species
identification and quantification of the percentage of parasitized red cells).
 Blood cultures: obtain two sets from two separate venipuncture sites.
 N.B: Widal test is of limited clinical utility in acutely ill patients because positive
results may represent previous salmonella infection.
  Urine analysis: shows pyuria, bacteruria and varying degree of hematuria in UTI.
Urine culture may reveal particular offending organisms with specific antibiotic
sensitivity.
 Stool analysis: gram stain and culture, microbiology for micro-organisms, pyuria,
RBCs and cytotoxin assay for c. difficile.
 Chest x ray: the presence of an infiltrate suggests pneumonia.
 Throat swab, wound swab for gram stain and culture when indicated.
 Lumber puncture in cases of suspected meningitis (once raised intracranial pressure
ruled out by lack of papilledema or a negative head CT scan study).
 Liver enzymes: serum aminotransferases would be very high in acute viral hepatitis.
 Ultrasound study of the abdomen in cases suspected of hepatic or biliary infections.

Management:
Reduce fever
 Use antipyretics; this also reduces systemic symptoms of headache, myalgias and
arthralgias.
 Paracetamol is generally preferred to nonsteroidal anti-inflammatory drugs (NSAIDs)
because of minimal adverse effects.
 Rapid reduction in body temperature can also be accomplished by cool or tepid (20
°C) sponges.
 If the patient cannot take oral antipyretics, use parenteral preparations of NSAIDs or
rectal suppositories of various antipyretics.
 Rehydration of the patient either orally or IV will help to reduce the temperature.

Malaria: see the protocol for malaria (appendix 1)

Respiratory tract infection:

 Viral URTI: offer symptomatic treatment (an antipyretic, antihistamine, antitussive
and a decongestant)
 Lower RTI: Community acquired pneumonia (CAP):
o The ability to determine a causative organism in most cases is low. Thus,
therapy for CAP is typically begun on an empiric basis.
o Assess the degree of severity upon historical risk factors, hemodynamic
parameters, physical and laboratory findings. Decide on need for
hospitalization.

Treatment of community acquired pneumonia (CAP) *

Patient Category Suggested Antibiotic Therapy

Outpatients (not severe) Amoxicillin; OR macrolide (erythromycin,
clarithrmycin) if penicillin-allergic
Hospitalized (not severe) For patients untreated previously in the community:
Amoxicillin OR macrolide: (erythromycin or
clarithromycin)
 For patients able to take oral medications: Oral
amoxicillin PLUS macrolide (erythromycin,
clarithromycin)
For patients requiring intravenous therapy: IV
penicillin or benzylpenicillin PLUS erythromycin or
clarithromycin
Hospitalized (severe) Amoxicillin-clavulanate or cefuroxime, cefotaxime,
ceftriaxone PLUS erythromycin or clarithromycin

* Re: British Thoracic Society Guidelines (2001)

Urinary Tract Infection (UTI):

 Assess the degree of severity upon historical risk factors, hemodynamic parameters,
physical and laboratory findings. Decide on need for hospitalization

 Acute cystitis:
o Offer a three-day course trimethoprim-sulfamethoxazole (TMP-SMX), a
fluoroquinolone or a week course of nitrofurantoin.
o Pregnancy: obtain a urine culture all pregnant women with acute cystitis. Use
amoxicillin, nitrofurantoin or cephalexin: each of these drugs is given for three
to seven days.

 Acute pyelonephritis:
o Outpatients: offer a week course of an oral fluoroquinolone (e.g.:
ciprofloxacin, norfloxacin), trimethoprim or TMP-SMX. Extend the duration
of treatment if the patient fails to respond adequately.
o Hospitalized patients: use ceftriaxone or gentamicin (3 to 5 mg/kg for patients
with normal renal function) given once daily. Modify according to urine
culture and particular organism sensitivity.

Acute Fever with Diarrhea:

 Attend to volume repletion (see “Shock” section). Use intravenous and oral route via
Oral Rehydration Salts.
 Specific antibiotic treatment is only indicated in certain situations:
o Bacillary dysentery: offer TMP/SMX or a quinolone course for 5 days.
o Enteric fever: treat with two week course of amoxicillin or ciprofloxacin.
o Amebic dysentery and amebic liver abscess: metronidazole for 5-10 days.

Acute Febrile CNS infections:

 Encephalitis: acyclovir for herpes simplex encephalitis.
 Meningitis:
o Treat adults with community-acquired meningitis empirically with
benzylpenicillin.
o Ceftriaxone and cefotaxime are alternatives if meningococcal resistance is
high.
o Treat for at least 5 days.
o Intravenous dexamethasone (0.15 mg/kg every six hours) may be also be
given in adults with suspected bacterial meningitis who have a Glasgow coma
score of 8 to 11 to reduce the chances of developing permanent neurological
deficits.
o Chemoprophylaxis needs to be considered for the index patient to eradicate
colonization and protect contacts. Offer rifampicin, a fluoroquinolone, or a
cephalosporin.
Table of drugs used in this section:

Drug Main Indication Recommended Dose

Paracetamol Pain or fever Oral, 1000 mg 3-4 times /day; rectal:
325-650 mg every 4-6 hours, do not
exceed 4 g/day.
Amoxicillin Susceptible 875 mg every 12 hours or 0.5- 1 gm every
respiratory and 8 hours
urinary tract
infections and
enteric fever
Erythromycin Susceptible Oral: base: 250-500 mg every 6-12 hours
respiratory tract
infections
Clarythromycin Susceptible Oral: 250-500 mg every 12 hours for 7-
respiratory tract 14 days
infections
Benzylpenicillin Susceptible I.M., I.V.: 2-24 million units/day in
respiratory divided doses every 4 hours depending
infections and on sensitivity of the organism and
meningitis severity of the infection
Cefuroxime Susceptible I.M., I.V.: 0.75-1.5 g every 8 hours (up to
respiratory 1.5 g every 6 hours in life-threatening
infections infections)
Trimethoprim- Urinary tract Oral: 1 double strength tablet every 12
sulfamethoxazole infection, bacillary hours for 10-14 days
dysentery

Nitrofurantoin Urinary tract Oral: 50-100 mg/dose every 6 hours (not

infection to exceed 400 mg/24 hours)
Ciprofloxacin Urinary tract Mild/moderate: oral 250 mg every 12
infection and hours for 7-14 days, I.V.: 200 mg every
enteric fever 12 hours for 7-14 days.
Severe/complicated: oral 500 mg every
12 hours for 7-14 days, I.V.: 400 mg
every 12 hours for 7-14 days
Metronidazole Amebiasis and Oral: 500-750 mg every 8 hours for 5-10
amebic liver days
abscess
Norfloxacin Urinary tract Oral: 400 mg twice daily for 3-21 days
infection depending on severity of infection or
organism sensitivity; maximum: 800
mg/day

Cefotaxime Urinary tract I.M., I.V.: 1-2 g every 8 hours

 infection
Acyclovir HSV encephalitis I.V.: 10 mg/kg/dose every 8 hours for 10-
15 days
Ceftriaxone Pneumonia, UTI, I.M., I.V.: 1-2 g every 12-24 hours
septicemia, (depending on the type and severity of
bone/joint infection); maximum: 4 g/day treatment
infection, or intra-
abdominal
infection
Meningitis I.V.: 2 g every 12 hours
Rifampicin Meningococcal Oral: 600 mg every 12 hours for 2 days
meningitis <1 month: 10 mg/kg/day in divided doses
prophylaxis every 12 hours for 2 days
Infants and Children: 20 mg/kg/day in
divided doses every 12 hours for 2 days

Approach to Headache in the Emergency Department (1)

 Approach to Headache in the Emergency Department (1)

?What is the reason for presentation

The patient can no longer :The headache is either

tolerate their typical recurrent The first headache of significant severity
headaches Or
.Sufficiently different or severe to alarm the patient .2

Obtain history and neurologic exam

Obtain history and neurologic exam

Features suggestive of a focal or infectious lesion

History typical Atypical history or
for migraine or focal abnormality
cluster on neurological
headache and exam
normal exam
:History
Headache of sudden rapid onset
Abortive therapy and observe Onset during exertion
History of altered mental status
Posterior radiation of headache
:Patient responds Patient does not First severe headache after 35
Probably primary respond; duration > Prior or co-existent infectious
headache, 48hrs; evidence of disease
discharge and volume-depletion or
follow up electrolyte disturbance :Examination
from prolonged Nuchal rigidity
vomiting Toxic appearing or fever
Papilledema
Any localizing or lateralizing
abnormality
Status Decreased mental status
migrainosus

Proceed to NEXT
FIGURE
 Approach to Headache in the Emergency Department (2)

Patients have none of the above Patients with one or more features-
features-Low risk category High risk category : CT/LP indicated

: Typical low risk patient History and physical History and physical examination
Age below 30 .1 examination more more concerning for intracranial
concerning for infection lesion/subarchnoid hemorrhage
History of previous headache .2
No worsening while in ER .3
Repeat exam normal .4 Noncontrast head CT

Abortive therapy Findings on physical examination

Normal Structural
Observe and repeat exam suggestive of need for CT prior to
LP (papilledema, focal neurologic lesion or
findings, altered mental status) bleed
visualized
Neurologic status normal, and Consider LP if
headache improving on repeat exam subarachnoid
NO YES hemorhage or
infection are in
the differential
diagnosis
Probable migraine or other
primary headache disorder.
.Discharge to care of family Neurosurgery
consult

Lumbar puncture ,Urgent CT prior to LP

Normal Large or posterior structural

image lesion or bleed visualized

,CSF WBCs RBCs tube #1 WBCs 5< RBCs in tubes #1&

few or no RBCs, no RBCs #3 or xanthochromia
probable CNS RBCs tube #3 normal glucose
infection ;No xanthochromia and CFS protein
Proboble traumatic tap

Treat with appropriate If deficits have Probable

antiviral or antibiotic Observe resolved, manage as subarachnoid
therapy acute migraine hemorrhage
 Approach to Medical Causes of Acute Abdominal Pain
Editor: Amira Abbas Mohamed Fadl

Introduction:
Many medical conditions can give rise to abdominal pain, and cause diagnostic confusion
with an acute (surgical) abdomen.
The acute abdominal pain may arise from: (1) stretching, (2) strong violent contraction,(3)
ischemia or infarction of the viscera, or from(4) muscle, (5)skin,(6) bone,(7) blood vessels
and(8) nerves overlying or adjacent to the abdomen.
In any patient presenting with abdominal pain careful history, examination, relevant
investigations are important, together as well when indicated a trial of medical therapy is
undertaken to avoid an unnecessary laparotomy.

Causes:
The following group of conditions should be considered:

1. Intrathoracic causes:
The lower six thoracic nerves supply both thorax and abdominal wall, as well as, the heart
and pericardium rest on the diaphragm, so thoracic pathology give rise to abdominal pain-
usually upper abdomen (epigastrium, left or right hypochondrium). Important causes are:
1. Myocardial infarction
2. Pericarditis.
3. Pulmonary embolus.
4. Pleurisy and pneumonia.

2. Intra-abdominal and retroperitoneal causes:

1. Congestion of the liver, occurring in CCF (congestive cardiac failure) and acute
hepatitis.
2. Acute pancreatitis
3. Acute pyelonephritis.
4. Bowel ischemia, which may be due to:
 Sickle cell disease.
 Henoch-Schonlein purpura
 Vasculitis as in PAN (polyarteritis nodosa), SLE (systemic lupus
erythematosis.
 Atherosclerosis of blood vessels.
5. Constipation. This may cause severe abdominal pain especially in elderly .Rectal
examination and plain abdominal x-ray will confirm this.
6. Infection:
 Gastroentritis, causes colic usually in association of diarrhea and vomiting.
 Worms: Tape worms can cause quite severe abdominal pain. Ova and cysts
should be looked for in stool analysis.
 Primary peritonitis: may occur in patients with ascites, as in portal
hypertension or nephritic syndrome.
 Typhoid fever.
 Mesenteric adenitis.
3- Metabolic and endocrine causes:
 Diabetic keto-acidosis.
 Hypercalcaemia.
 Acute intermittent Porphyria.
 Addison’s disease and crises.
 Heavy metal poisoning, such as lead toxicity.

4- Neurogenic causes:
 Root pain such as compression from degenerativelesions or malignancy. The pain is
commonly described as a band coming from back to front, associated with tenderness
over involved vertebrae when examining patient back.
 Tabes dorsalis: the presence of Argyll Robertson pupils(irregular pupils reactive to
accommodation but not to light).
 Herpes zoster: usually pain and paraesthesia precede the rash before few days.It is
usually unilateral and segmental.
 Psychiatric causes: such as Munchausen’s syndrome: such patients present with
convincing symptoms and signs of various acute conditions especially involving the
abdomen.

Investigations:
Depending on the most likely possibility as obtained from history and examination, the
relevant investigation from the list below are carried out:
1. Plain supine abdominal x-ray.
2. Erect chest x-ray.
3. Blood film.
4. Urine general.
5. Stool general.
6. Ascitic fluid analysis gram stain and culture.
7. Widal test for typhoid.
8. Serum amylase.
9. ECG.
10. Radiological studies such as U/S abdomen, Doppler studies of vessels or
contrast studies.

Management:
Largely depends on the underlying diagnosis.
Various General Medical
Emergencies
 Shock
Editors: Elwaleed Ali and Mohammad Al-Baqir

Definition:
Shock is a pathological state characterised by significant reduction in systemic tissue
perfusion which results in decreased tissue oxygen delivery. If not reversed early and
adequately it may lead to:
1. Cellular hypoxia.
2. Disruption of critical biochemical processes and may eventually lead to:
 Cell membrane ion pumps dysfunction.
 Intra cellular edema.
 Inadequate regulation of intercellular pH.
 Cell death.

For management purposes, shock is divided into two types: hypovolemic shock and
distributive shock.

Hypovolemic Shock

Definition
o Hypovolemic shock is caused by decreased circulatory volume manifesting in tissue
hypoperfusion.
o Common precipitants are blood loss (internal or external bleeding) or fluid-loss, e.g.
vomiting, diarrhea, burns or sequestration as in pancreatitis.

Management:
o Insert two large-bore cannulae (14 or 16 gauge) into large veins. Central venous
cannulation or cut-down might be utilized if peripheral veins are inaccessible.
o Infuse one to two liters of isotonic saline or lactated Ringer’s as rapidly as possible.
o Continue fluid repletion at the initial rapid rate as long as the systemic blood pressure
remains low.
o Monitor clinical signs, including blood pressure, urine output, mental status, and
peripheral perfusion. These are often adequate to guide resuscitation.
o The development of peripheral edema is often due to acute dilutional
hypoalbuminemia and should not be used as a marker for adequate fluid resuscitation
or fluid overload.
o Colloids stay longer within the intravascular compartment and are replaced 1:1 with
blood. However, they do not reduce mortality, are not more effective in preserving
pulmonary function and are much more expensive than crystalloid fluids.
o Consider blood products in hemorrhagic shock. Type-specific or O negative packed
red blood cells (PRBC) are given to maintain the hematocrit above 30%.
 o Whole blood provides extra volume and clotting factors. Transfuse fresh frozen
plasma and platelets when:
 Coagulation studies are abnormal
 Platelet count is < 10,000/µL
 After transfusion of 6 or more units of PRBCs

Distributive Shock

Definition
o Distributive shock refers to shock caused by arterial and venous dilatation with low
systemic vascular resistance.
o It usually arises from sepsis, anaphylaxis or systemic inflammatory response
syndrome (SIRS) produced by severe pancreatitis or burns.
o Sepsis is the most common cause and carries a mortality of 40-80%.
o Typically patients present with fever, chills, hypotension, hyperglycemia and altered
mental status mostly due to gram negative bactremia.
o Effective treatment of septic shock requires resuscitation, supportive care, monitoring,
and targeted antimicrobial therapy and drainage for infection.

Management:
Resuscitation:

o Assess and support the airway, respiration, and perfusion. Supplement oxygen to all
patients with sepsis, monitor oxygenation with continuous pulse oximetry. Intubation
may be required for airway protection because of encephalopathy or a depressed level
of consciousness complicating sepsis.
o Administer fluids in well-defined, rapidly infused boluses. Monitor volume status,
(pulse rate, blood pressure, urine output, central venous pressure or pulmonary
capillary wedge pressure if feasible) and look for features of pulmonary edema before
and after each bolus. Repeat intravenous fluid challenges until hemodynamic
parameters are acceptable or features suggestive of pulmonary edema develop. If the
pulmonary capillary wedge pressure is monitored, do not exceed 18 mmHg.
o Clinical trials have not consistently demonstrated an advantage of colloid over
crystalloid infusion in the treatment of septic shock. Therefore, crystalloids are
preferred.

Vasopressors:

o Vasopressors are useful in patients who remain hypotensive despite adequate fluid
resuscitation or who develop cardiogenic pulmonary edema.
o In general, agents that augment peripheral vascular resistance, such as dopamine,
norepinephrine, or phenylephrine, are required for initial stabilization

Source Control:

o Prompt identification and treatment of the culprit site of infection are essential.
 o Potential Gram negative pathogens are generally best covered with two effective
agents from different antibiotic classes, usually a beta-lactam and an aminoglycoside
(eg, a third generation cephalosporin such as ceftazidime and gentamicin).
o Antibiotics should be appropriately tailored once microbiological data returns.
o Regardless of the antibiotic regimen selected, patients should be observed closely for
toxicity, evidence of response, and the development of nosocomial superinfection.
o The duration of therapy depends upon the source of the infection and the clinical
response of the patient.
o Corticosteroids are life-saving in the treatment of shock associated with acute adrenal
insufficiency, but they are of no benefit in other types of shock.

For (Cardiogenic Shock), please refer to Cardiovascular Emergencies section

Drugs used in this section:
Drug Indication Recommended Dose
Gentamicin Hemodynami Susceptible systemic infections: I.M., I.V.: Severe
c support in life-threatening infections: 2-2.5 mg/kg/dose every 8
septic shock hours
Note: High-dose, once daily regimens: Some
clinicians suggest 4-7 mg/kg (as a single daily dose)
for all patients with normal renal function. This dose
is at least as efficacious with similar, if not less,
toxicity than conventional dosing.
Phenylephrine Hemodynami I.M., S.C. : 2-5 mg/dose every 1-2 hours as needed
c support in (initial dose should not exceed 5 mg)
shock I.V. bolus: 0.1-0.5 mg/dose every 10-15 minutes as
needed (initial dose should not exceed 0.5 mg)
I.V. infusion: 10 mg in 250 mL D5W or NS (1:25,000
dilution) (40 mcg/mL); start at 100-180 mcg/minute
(2-5 mL/minute; 50-90 drops/minute) initially; when
blood pressure is stabilized, maintenance rate: 40-60
mcg/minute (20-30 drops/minute); rates up to 360
mcg/minute have been reported; dosing range: 0.4-
9.1 mcg/kg/minute
Norepinephrin Hemodynami Continuous I.V. infusion:
e c support in Adults: Initial: 0.5-1 mcg/minute and titrate to
shock desired response; 8-30 mcg/minute is usual range;
ACLS dosing range: 0.5-30 mcg/minute
Rate of infusion: 4 mg in 500 mL D5W
o 2 mcg/minute = 15 mL/hour
o 4 mcg/minute = 30 mL/hour
o 6 mcg/minute = 45 mL/hour
o 8 mcg/minute = 60 mL/hour
o 10 mcg/minute = 75 mL/hour
Dopamine Hemodynami I.V. infusion: 1-5 mcg/kg/minute up to 50
c support in mcg/kg/minute, titrate to desired response; infusion
shock may be increased by 1-4 mcg/kg/minute at 10- to 30-
minute intervals until optimal response is obtained
Note: If dosages >20-30 mcg/kg/minute are needed, a
more direct-acting vasopressor may be more
beneficial (ie, epinephrine, norepinephrine).
Hemodynamic effects of dopamine are dose
dependent:
o Low-dose: 1-5 mcg/kg/minute, increased renal
blood flow and urine output
o Intermediate-dose: 5-15 mcg/kg/minute,
increased renal blood flow, heart rate, cardiac
contractility, and cardiac output
o High-dose: >15 mcg/kg/minute, alpha-adrenergic
effects begin to predominate, vasoconstriction,
 increased blood pressure
Ceftriaxone Septic shock I.M., I.V.: 1-2 g every 12-24 hours (depending on the
type and severity of infection); maximum: 4 g/day

Coma
Editor: Elwaleed Ali Mohamed Elhassan

Definition:
Coma is a state of unresponsiveness to normal external stimuli.

Causes:
The causes of coma can generally be divided into:
Coma without focal or lateralizing neurological deficits:
 Metabolic e.g.: hypo and hyperglycemia, uremic encephalopathy, hepatic failure and
thiamine deficiency
 Endocrine e.g.: hypo and hyperthyroidism and adrenal insufficiency
 Electrolyte disturbances: hypo and hypernatremia and hypercalcemia.
 Alcohol, ingested drugs and toxins e.g.: opiates, benzodiazepines, barbiturates and
carbon monoxide.
 Hypo and hyperthermia.
 Epilepsy.
 Hypertensive encephalopathy.

Coma with focal or lateralizing neurological signs (due to brainstem or cerebral dysfunction):
 Cerebrovascular accidents
 Space occupying lesion: (tumor, hematoma or abscess). In order to produce coma
these have to be within the brainstem or compress it by producing brain shift

Coma with meningeal irritation:

 Meningitis
 Encephalitis
 Subarachnoid hemorrhage.
 Cerebral malaria

Management:
 Ascertain a patent airway and adequate respiration. Supplement with oxygen and intubate
if necessary to protect the airway (see “Shock” section).
 Quickly assess circulation, record pulse and blood pressure
 Place patient on a cardiac monitor if feasible.
 Insert a peripheral intravenous access and obtain samples for appropriate investigations:
 Blood film for malaria.
 Complete blood count with differential
 Finger-stick and blood glucose
 Hepatic, renal profiles and electrolytes
 Urinalysis
 Administer IV fluids as needed for hypotension
 Give dextrose (50 ml of 50%) immediately if hypoglycemia is proved or suspected.
 Control seizures if present (see “Status Epilepticus” section)
 Reduce high temperature if present with tepid sponging and antipyretics.
 Take a quick history from relatives and attendants:
o Onset of coma?
o Any observed seizures?
o Recent complaints: headache, fever, vertigo (etc)
o Recent medical history: sinusitis, otitis, neurosurgery (etc)
o Past medical history: diabetes mellitus, hypertension, epilepsy, head trauma.
o Drug or toxins exposure: alcohol, benzodiazepines, opiates...
 Examine the patient:
o Assess and record the Glasgow Coma Scale (GCS) for objective follow-up.
o Look for signs of trauma in the head (hematoma, CSF or blood in the nose or ears) or
body.
o Look for stigmata of other illnesses: liver disease, alcoholism, DM, myxedema.
o Note the pattern of respiration and smell the breath for fetor hepaticus, ketosis,
uremia)
o Test for meningeal irritation; do not move the neck unless the cervical spine is
cleared.
o Examine the heart and lungs for murmurs, rubs, wheezing and collapse
o Examine the abdominal organs, look for ascites, peritonism.
o Examine the pupils, ocular fundi, brainstem reflexes and eye movements. Look for
local deficits and examine plantar reflexes.
 Further investigations may be needed based upon the clues gathered from above:
o Obtain a head CT scan for all undiagnosed coma patients and those with focal
neurological signs.
o Perform a lumbar puncture and CSF analysis in cases suspected of meningitis or
subarachnoid hemorrhage. Avoid in the presence of papilledema.
 Transfer the patient to the ICU or a special care room if feasible
 Monitor fluid balance with input and output chart. Insert an indwelling catheter if needed
for hemodynamic status monitoring.
 Avoid nasogastric tube insertion if airway reflexes are impaired unless the patient is
intubated.
 Attend to nursing care measures
 Provide further specific therapeutic interventions once underlying cause is identified. See
“Drug Overdose and Poisoning” section below, refer to other relevant sections.
Approach to Drug Overdose and Poisoning
Editor:Elwaleed Ali Mohamed Elhassan
 Emergency Department Approach to Drug Overdose and Poisoning

Rapid evaluation and stabilization

Airway Breathing Circulation

Supplement O2 Establish IV access

Consider intubation if patient has altered Place patient on a monitor.
mental status, or is at risk for aspiration or Administer IV fluids as needed
respiratory failure. for hypotension

Check mental status

Disturbed or frankly Normal

comatose

Consider giving:
IV thiamine 100 mg
Dextrose (50 mL of a 50 % solution)
IV naloxone (0.4 to 2.0 mg) if suspected opiate
overdose

Obtain history from patient and family:

Substances taken
Time of ingestion
Associated alcohol consumption
Current medical conditions and medications
Psychiatric history
Was overdose intentional or accidental
Note: history may be unreliable!
 Physical Examination

Pay special Attention to:

Characteristic odors
Mental status alterations
Blood pressure, heart and respiratory rate alterations
Temperature alterations
Pupillary findings
Skin findings

Helpful hints are exemplified by:

Dilated pupils: tricyclics, amphetamine, glutethimide, cocaine
and anti-cholinergics
Pinpoint pupils: opiates (e.g. pethidine, morphine ,
diphenoxylate (lomotil) and organophosphates
Nystagmus: alcohol, benzodiazepines and phenytoin.
Nasal bleeding or peri-oral sores: solvent abuse
Hyperventilation: salicylate

Perform the following investigations:

Send blood samples for: CBC, BUN, Cr, electrolytes.
If available, obtain serum and urine toxicology screens,
paracetamol and salicylate levels.
Obtain ECG
Consider liver function tests, serum osmolality, arterial
blood gases and CXR.
 Management

General measures Specific measures Particular

antidotes
if
available

G.I. decontamination: Hemodialysis: Forced alkaline diuresis:

Mostly effective when Useful for Consider for salicylate
done within 60 minutes of water and phenobarbital
ingestion soluble Hazardous as may lead
For small and moderate toxin: to pulmonary edema
ingestions activated (ethanol, and electrolyte
charcoal alone is mostly lithium, disturbances.
effective salicylate, Use 3 ampoules of Na
Should generally be methanol) bicarbonate in 1 L
avoided in patients with D5W-keep urine pH
depressed mental status 7.5-8.5; output at 2-4
(unless intubated) and ml/kg/hr.
those who took corrosives

Emesis: Activated charcoal: Gastric lavage:

A simple pre- Administer 60 to 100 Place patient in the left
hospital g mixed with water lateral decubitus
intervention. or sorbitol by mouth position with the head in
Give syrup or nasogastric tube. a 15° Trendelenburg
ipecac, 30 ml Dose may be position.
followed by a repeated. Remove stomach
big glass of Avoid in patients contents, irrigate by
water. with ileus or those in gravitational instillation
Repeat after 20 whom endoscopy is and drain several times,
mintues if planned use warmed normal
necessary saline or tap water.
Continue lavage until
the effluent is relatively
clear; 2-4 liters of fluid
are usually sufficient.
Cardiovascular
Emergencies
Editor:Ahmed Ali Ahmed Sulmian
 Acute Coronary Syndromes

This is defined as any collection of clinical symptoms, most commonly including chest pain,
that are compatible with acute myocardial ischemia. It is usually caused by atherosclerotic
coronary artery disease (CAD). It has two major components:

1. ST elevation myocardial infarction (STEMI). This is caused by total of occlusion of a

coronary artery by a thrombus leading to total cutoff of blood supply and infarction of
myocardium

2. Unstable angina (UA) and Non -ST elevation Myocardial Infarction (NSTEMI) .This
is caused by subtotal (near total) occlusion of a coronary artery by a thrombus leading
to critical ischemia +/- micro-infarction of the myocardium. If cardiac markers are
elevated (CKMB or troponin) it is called Non-ST elevation myocardial infarction.
However, management is the same and hence grouped together.

Evaluation of patients with suspected ACS:

Any patient who presents with new onset prolonged chest pain (>10 min) at rest or with
minimal exertion should be evaluated for ACS. Patients with prior CAD, patients with risk
factors like diabetes, mellitus (DM), hypertension, smoking, etc., or have chest pain
associated with nausea, vomiting, shortness of breath or chest pain accompanied by
pulmonary edema are more likely to have an acute coronary syndrome.

The following steps should be taken:

1- A cardiac history and examination should be rapidly performed. Ask about risk
factors and history of prior CAD.
2- Attach the patient to a (rhythm) monitor and obtain an immediate ECG. The ECG will
divide patients into 3 categories
a) New or presumed new ST segemnt elevation greater than 0.1 mV(1 mm) in at
least 2 contiguous precordial leads or 2 adjacent limb leads) or new or
presumed new Left Bundle Branch Block (LBBB). This is ST-elevation
myocardial infarction.(Manage as below)

b) Patients with transient ST deviation (≥.5mm) or deep T wave inversion

(≥2mm) are considered high risk for UA/NSTEMI. These should be managed
as UA/STEMI as below.

c) Normal or non-specific (e.g. ST deviation < 1mm, flat T waves) ECG. These
should be admitted to a monitored unit and UA/NSTEMI treatment started
with serial ECGs and cardiac markers (CKMB and troponin) obtained 6-12
hours apart. If cardiac markers and ECGs are normal stress test before or soon
after discharge should be performed or referral to a tertiary facility where
stress test can be formed.
 3- Draw blood for cardiac enzymes (CK, CKMB, troponin I or T), random blood sugar,
serum potassium, urea and creatinine, complete blood count.
4- Obtain Chest X-ray if portable X-ray is available or patient can be moved with a
monitor.

Management:
The following steps should be taken in all patients with ST-elevation myocardial infarction or
Unstable Angina/ Non-ST elevation myocardial infarction.

 Admit to CCU. Establish IV access.

 Bed rest with continuous ECG monitoring.
 Supplemental O2 to via nasal cannula at a rate of 4-6L /min to maintain O2sat > 90%
and at times of chest pain.
 Aspirin 300 mg to crush and swallow then 100-300 mg daily.
 Nitrates. If there is ongoing chest pain give sublingual nitrates- isosorbide dinitrate or
glyceryl trinitrate. Oral or IV nitrates if pain is continuous or there is associated high
blood pressure or pulmonary edema.
 Analgesia. Morphine IV for pain, anxiety or pulmonary edema. IV morphine sulphate
4-6 mg every 5 -15 min as needed. Give metoclopramide 10 mg IV or IM for nausea
and vomiting.
 Beta blockers, oral or IV. Use short acting agents like propranolol or metoprolol. Give
B blockers to all patients unless there is a contraindication. Aim to reduce heart rate to
about 60-70/min.
 Strict glycemic control in diabetic patients. Regular/soluble Insulin infusion pump is
preferred otherwise SC regular/soluble insulin 6-8 hourly +/- initial IV
soluble/regular insulin bolus to keep blood sugar preferably between 80-160 ( and not
beyond 200 mg/dl)

Management specific to ST Elevation myocardial infarction:

 All patients with STEMI should receive thrombolysis as urgently as possible if they
satisfy the following 3 criteria:
I. There is prolonged chest pain more than 10 min and new or presumed new ST
segment elevation greater than 0.1 mV(1 mm) in at least 2 contiguous
precordial leads or 2 adjacent limb leads or new or presumed new Left Bundle
Branch Block (LBBB).
II. Arrival within 12 hours of the start of the pain
III. Absence of absolute contraindications to thrombolysis.
Absolute contraindications: 1- Intracranial hemorrhage at any time 2-known structural
vascular lesion eg arteriovenous malformations (AVM) 3- Any ischemic stroke within last 3
months 4-Primary or metastatic cerebral malignant tumor 4-Suspected aortic dissection 5-
Active bleeding or bleeding disorder excluding menses 6-Significant head or facial trauma
last 3 months.
Patients with relative contraindications have higher risk of intracranial bleeding than other
patients. Risk of bleeding from thrombolysis has to be weighed against risk of death of MI.
Two factors favor administering thrombolysis. First, presence of high risk markers for death
from MI( large anterior infarct involving most or all precordial leads, hemodynamic
instability, diabetes, pulmonary edema, electrical instability ie sustained or nonsustained VT)
and support services in the hospital including ability to adequately monitor patients,
accessibility of blood products like fresh frozen plasma(or cryoprecipitate or fresh blood),
platelet transfusion and protamine sulphate to reverse anticoagulation, neurosurgical support,
ability to endoscope rapidly if GI bleed occurs etc..

Streptokinase, alteplase, reteplase, tenecteplase,etc. can be used.

 IV Heparin
Unfractionated heparin is indicated in
I. In patients who have received alteplase, reteplase or tenecteplase.
II. In patients who have received non selective thrombolyic agent like streptokinase
or who have not recieved thrombolysis who are at high risk for systemic emboli
these are large or anterior MI, A fib, previous embolic event, or known LV
thrombus.

LMWH can be used instead. Enoxaparin is the preferred agent.

Management specific for Unstable Angina/Non-ST elevation myocardial

infarction(UA/NSTEMI)

 Heparin IV in all patients either unfractionated heparin or LMWH for 48-72 hours
after symptoms subside.
 Clopidogrel (Plavix) in patients allergic or intolerant to aspirin or as added on therapy
in high risk patients. Give 300 mg orally as loading dose then 75 mg orally daily.
 Angiotensin converting enzyme inhibitors in diabetic patients, patients with
pulmonary edema, hypertension or impaired left ventricular systolic function.
 Platelet GP IIb/IIIa receptor inhibitors in high risk patients and prior to catheter
 Coronary angiography. Patients with refractory chest pain and ECG changes or
elevated cardiac markers despite maximum medical therapy should be referred for
immediate coronary angiography if feasible. Otherwise, high risk (ECG changes or
elevated markers) patients can be transferred after stabilization.
 Acute Cardiogenic Pulmonary Edema
Definition:
Acute pulmonary edema is a clinical condition characterized by the onset of acute shortness
of breath due to pulmonary vascular congestion .This occurs secondary to elevated left atrial
pressures either from mitral valve disease or elevated left ventricular end-diastolic pressure
due systolic or diastolic dysfunction.

Diagnosis and clinical evaluation:

Acute cardiogenic pulmonary edema is diagnosed clinically by the presence of acute
shortness of breath and one of the following:
1- Clinical evidence of pulmonary congestion that is coarse crepitations at the lung bases
extending apically +/- wheezes.
2- Radiological evidence of pulmonary edema *
I- Prominent upper lobe vessels. Upper lobe vessels appear much larger than
lower lobe vessels due to flow redistribution.
II- Interstitial edema in the form of Kerley B lines (sharp, linear densities of
interlobular interstitial edema found in the lower lung fields peripherally
and usually extending to the pleural surface), Kerly A lines (linear
densities emanating from the hila to the lung parenchyma) associated with
blurring of the pulmonary vessels.
III- Alveolar edema seen as bilateral perihilar infiltrate in a butterfly pattern.
Pleural effusions may be seen.

Investigations:
ECG
 First exclude ST elevation myocardial infarction.
 Then look for ECG abnormalities that might suggest the etiology of heart
failure:
- ST segment depression +/- T wave inversion suggesting ischemia
- M mitrale +/- RVH and P pulmonale suggesting mitral valve disease,
- LVH suggesting long standing hypertension or aortic valve disease, etc.

Chest X-ray
1- Look for evidence of pulmonary edema as above taking into account that there
may be a lag of several hours between clinical and radiological findings.
2- Examine cardiac silhouette. Look for cardiomegaly and any other abnormalities
eg evidence of mitral valve disease (straightening of the left superior cardiac
border carinal widening > 90 degrees and 'double right heart border' due to
superimposed dilated left atrium on the right atrium).
3- Make sure to exclude other non-cardiac conditions that cause shortness of breath
e.g. pneumothorax, massive pleural effusion, etc.

Blood tests:

1- Check renal function. Blood urea, serum creatinine and potassium.

2- Hemoglobin level if patient looks pale.
 3- Cardiac enzymes: CK, CK MB and troponins in patients over 40 yrs or at risk
for ischemic heart disease.
4- Other tests as clinically indicated e.g. thyroid function tests if
hyper/hypothyroidism suspected.

Treatment:

1. Place patient in sitting position. Admit to monitored unit if available.

2. Oxygen: Administer oxygen preferably by nasal cannula at 4- 6 L/min. Alternatively
use face mask starting with 100% oxygen.. Oxygen therapy is better guided by pulse
oximetery to keep O2 saturation ≥90 %.
3. Diuresis: Use intravenous loop diuretics. Furosemide at dose of 0.5-1 mg/kg IV bolus
(usually 40 -80 mg). If no diuresis within 1 hour double the dose or use continuous IV
infusion.
4. Morphine sulphate: Give 4-6 mg IV by slow IV push over 2-3 min. Repeat every 5-15
min as needed. Do not oversedate patient.

Additional therapy:
Nitrates
Nitrates are indicated in pulmonary edema in patients with systolic BP above 100 mmHg and:
1- without prompt relief of symptoms with IV diuretics.
2- high blood pressure.
3- angina or other evidence of ischemia.

Start by sublingual nitrates then start IV nitrates if needed. Check IV glycerltrinitrate dosage
below.

ACE inhibitors:
ACE inhibitors should be started during the same admission. Start with captopril 6.25 mg PO
TDS. Beware of first dose hypotension. Check BP at least once within the first hour after
captopril initiation. IF dose is tolerated increase dose every 24-72 hrs if BP stable.
Angiotensin receptor blockers like candesartan and losartan can be used if patient is
intolerant of ACE-I.

Digoxin
In acute pulmonary edema digoxin is indicated for patients with associated fast atrial
fibrillation or patients with recurrent relapses of pulmonary edema. IV digoxin is indicated in
patients with severe pulmonary edema and fast atrial fibrillation.Check Patient has to be on a
monitor and serum potassium corrected to ≥3.5meq/l.
For dosage refer to table below.
 Acute Cardiogenic Pulmonary Edema

Step 1

Diagnosis
Patient presents with acute breathlessness+ evidence of
pulmonary congestion.

Step 2

Investigations
-CXR
-ECG
-Blood test: urea, electrolytes, Hb and cardiac enzymes

Step 3
Treatment
Admit patient to monitored unit if possible.
Supplemental oxygen
IV frusemide
Morphine sulphate

Step 4

Additional therapy
Consider use of:
1- Nitrates: Sublingual or IV.
2- Digoxin oral or IV
3- ACE-I.
 Cardiogenic Shock
Definition
Cardiogenic shock is a low output state characterized by elevated ventricular filling pressures
and low cardiac output. This is recognized clinically by presence of pulmonary edema and
persistent systemic hypotension (SBP<90) for more than 30 min and evidence of vital organ
hypoperfusion (e.g. confusion, cold extremities, oliguria). It carries dismal prognosis with
very high mortality. It most commonly occurs in patients who have sustained considerable
myocardial damage after a large myocardial infarction or may occur in patients with
mechanical complications like post MI ventricular septal defect (VSD) or acute severe
valvular regurgitation or in patients with very advanced congestive heart failure.

Management

1. Administer supplemental oxygen.

2. Blood pressure support. This is achieved by use of inotropic agents. The choice of the
inotropic agent depends on the BP and clinical state of the patient:
 If SBP is 60-90 mmHg and NO signs/symptoms of shock  Dobutamine is
the inotrope of choice at a dose of 2.5-20 mcg/kg/min IV. Start at a low dose
and use increments of 2.5 mcg/kg/min 15-30 min apart to achieve BP ≥ 100
mmHg.
 If dobutamine is not available use dopamine.
 If SBP is 60- 90 mmHg with symptoms or signs of shock  dopamine at a
dose of 5-15 mcg/kg/min. Use increments of 2.5 mcg/kg/min every 15-30 min
to achieve SBP ≥ 100 mmHg.
 If SBP < 60 mmHg  adrenaline or noreadrenaline at 0.5-30 mcg/min.

3. IV Furosemide preferably by infusion to relieve the pulmonary edema.

4. Intra-aortic balloon pump counterpulsation if available.
5. Correction of underlying cause. If cardiogenic shock occurs in the context of acute MI
administer reperfusion therapy whether via thrombolysis or primary angioplasty. In
patients with mechanical complications like ventricular septal defect (VSD) or acute
severe mitral or aortic regurgitation whether following MI, endocarditis, aortic
dissection, immediate cardiac surgery consultation or referral to a center with cardiac
surgery facility.
Drugs used in this section:

Drug Main Indication Recommended Dose

Streptokinase Acute Coronary Syndrome. 1.5 million units IV over 30-60
min

Reteplase Absolute contraindications for 10 units IV over 2 min then 30

thrombolytic therapy: min later another 10 units IV
(1) Intracranial hemorrhage at any over 2 min
time (2)known structural vascular
lesion e.g. AVM (3) Any ischemic
stroke within last 3 months
(4)Primary or metastatic cerebral
Alteplase 15 mg IV bolus, then 0.75
malignant tumor (5)Suspected aortic
mg/kg over 30 min(max 50 mg)
dissection (6) Active bleeding or
then 0.5 mg/kg over 60 min
bleeding disorder excluding menses
(not to exceed 35 mg)
(7)Significant head or facial trauma
last 3 months.
Aspirin Acute Coronary Syndrome. Initial dose 300 mg (nonenteric
formulation) followed by 100
Contraindications are allergy and mg/day.
active bleeding including retinal
bleeding.
Clopidogrel Acute Coronary Syndrome. 75 mg/d; loading dose of 4-8
(Plavix) tablets (300-600mg) can be
(Use if ASA is contraindicated) used for rapid action.
Unfractionated Acute Coronary Syndrome. 60 U/kg IV bolus (max 5000 U)
Heparin followed by 15 U/kg/hr (max
Stop if major bleeding occurs or if 1000/hr). Adjust rate to aPTT
platelet count drops below 100,000 60-80s.
(consider heparin-induced
thrombocytopenia). Reverse with
protamine sulphate
Enoxaparin Acute Coronary Syndrome. 10 U (1 mg)/kg SC twice daily.
An initial bolus 30 mg IV can
This is a low molecular weight be given.
heparin.
Similar contraindications as
unfractionated heparin.
Isosorbide Acute Coronary Syndrome. 10-40 mg PO BD or TDS
mononitrate
Nitrates are contraindicated in
hypotensive patients. Caution in
patients with inferior infarct
especially when given with B
blockers as severe hypotension may
 ensue in patients with concomitant
right ventricular infarct.
Isosorbide Acute Coronary Syndrome Sublingual: 5mg as needed.
dinitrate Repeat every 5 min X 3 doses.
Oral: 10 -20 mg BD or TDS
IV: Mix with D5w. 1-10 mg/hr
Glyceryl Acute Coronary Syndrome Sublingual: 0.5 mg every 5 min
trinitrate as needed x 3 doses.
IV: 10-200µg/min
Propranolol Acute Coronary Syndrome 10-80(usually 20-40 mg) mg
orally 2-3 times daily. For IV
Titrate dose to a resting heart rate use give 0.5-1 mg IV followed 2
60-70 bpm. hrs later with the oral dose.
Contraindicated in patients with
bradycardia < 60bpm, hypotension,
severe asthma or chronic obstructive
airway disease and pulmonary
edema.
Endocrine Emergencies

Editor: Hisham Abdel Rahim

 Diabetic Ketoacidosis (DKA)
Essentials of diagnosis:
1- Hyperglycamia i.e. blood glucose > 250 mg/dl.
2- Ketonaemia.
3- Ketonuria > +2 ketonuria
4- Metabolic acidosis: PH < 7.30.
Therefore DKA consists of the biochemical triad of hyperglycaemia, ketonemia and
acidaemia.

Differential diagnosis:
1. Alcoholic ketoacidosis.
2. Starvation ketosis.
3. Lactic acidosis.
4. Uraemic acidosis.
5. Salicylate intoxication.
6. Methanol intoxication.

Clinical Presentation
 Polyuria and polydipsia
 Nausea, vomiting and abdominal pain
 Hypovolemia (decreased skin turgor, dry axillae and oral mucosa, low jugular venous
pressure, and, if severe, hypotension)
 Kussmaul’s respirations (deep rapid breaths) with acetone odor.
 Disturbed mental status progressing to stupor and coma

Precipitating factors:
1- It may be the initial presentation of type 1 DM.
2- Omission of insulin.
3- Underlying infection and/or sepsis.
4- Acute coronary syndrome.
5- Stroke.
6- Trauma, pregnancy, surgery or drugs (e.g. corticosteroids and higher dose thiazides).

Diagnostic studies:
 Random blood sugar, urea, Na+, K+.
 Hemoglobin and white cell count.
 ECG
 Urine general.
 ABG, CXR
 Brain CT if indicated.
 Blood and urine culture.

Treatment:
Is best carried out at ICU if feasible:
 IV fluids.
 IV insulin.
  IV potassium chloride.
 Bicarbonate therapy

(A) IV fluids:
Give the following in succession:
 1 litre of normal saline over 30 minutes.
 1 litre of normal saline over one hour.
 1 litre of normal saline over two hours
 Then 500 ml of normal saline every 4 hours for the first 24 hours.
Substitute 5% dextrose in normal saline for normal saline when blood glucose drops below
250 mg/dl.
Observe urine output closely and keep an open eye to avoid volume overload in elderly
patient and patients with congestive heart failure or renal failure when central venous
monitoring is preferable.

(B) Insulin therapy:

 Administer 10 units of soluble insulin IV immediately, followed by a continuous
IV soluble insulin infusion at a rate of 5 units /hour till the patient is out of DKA.
 If IV infusion pump is not available soluble insulin can be given as 10 units IV
stat and 5-10 units IM every hour till the patient is out of DKA.
 It is preferable to have serum K+ result before giving IV soluble insulin. If the
patient is hypokalemia avoid IV insulin till hypokalemia is corrected.
 Monitor blood glucose hourly and ensure the addition of IV dextrose to the
planned IV fluid when blood glucose result drops below 250 mg/dl.

(C) Potassium replacement:

 If the initial serum potassium is < 3.3 mmol/L, hold insulin and give 40 mmol
potassium chloride as an infusion through a central venous line over one hour
until K > 3.3 mmol/L
 If serum K+ > 5.5 mmol/L do not give potassium. However, check serum K+ after
two hours.
 If serum K+ > 3.3 mmol/L < 5.5 mmol/L give 20 to 30 mmol of potassium
chloride in each litre of IV fluid to keep serum K+ at 4 – 5 mmol/L.
 Monitoring serum K+ every 4 to 6 hours.
 Continue with oral potassium for 5 to 7 days to restore total body potassium level.
(D) Bicarbonate therapy : -
 If PH > 7.0 no need for bicarbonate therapy.
 If PH 6.9-7.0  dilute sodium bicarbonate 50 mmol in 200 ml H2O and infuse at a
rate of 200 ml/hour.
 If PH < 6.9  dilute sodium bicarbonate 100 mmol in 400
 Repeat bicarbonate administration every two hours until PH > 7.0.
 NB: monitor serum K+ since it is likely to drop with IV bicarbonate.


Features of resolution of DKA:

 Blood glucose < 200 mg/dl/
 Serum HCO3 > 18 mmol/l
 Venous PH > 7.3
 If there is an obvious precipitating cause such as sepsis, acute myocardial infarction the
management of the DKA should include measures to control the precipitation factor e.g.
broad spectrum antibiotics for sepsis.
 If serum glucose does not fall by 50-70 mg/dl in the first hour double the dose of the IV
insulin till serum glucose fall by 50-70 mg/dl/h.
 If intramuscular insulin regimen in used and blood glucose does not fall by 50-70 mg/dl
in first two hours give IV soluble insulin (10) units as a bolus every hour till blood
glucose fall by 50-70 mg/dl/h.
 After resolution of DKA start SC soluble insulin every (4) hours while monitoring blood
glucose OR resume the original daily dose of insulin. In case of new onset of type 1 DM
the total daily insulin requirement can be estimated as 0.6 units/kg/day. This calculated
dose can be divided to be given every (4) hours.
 Start the subcutaneously soluble insulin regimen before the discontinuation of intravenous
insulin in order to prevent the redevelopment of DKA.

Complications of treatment:
 Hypoglycemia
 Hypo and hyperkalemia
 Pulmonary edema
 Cerebral edema, renal failure, ARDS, systemic thromboembolism

Notes

DKA Flow Sheet Setup

Time Vital Urine pH HCO3 Anion Ketones Glucose K Intravenous Insulin

Signs Outpu Gap Fluids
t
 Hyperosmolar Nonketotic Coma

Definition
 Hyperosmolar nonketotic coma is a state of extreme hyperglycemia (> 600mg/dL)
and hyperosmolality (>310 mOsm/L) in the absence of acidosis (pH >7.3, HCO3 > 15
meq/L) that is mostly seen in type 2 diabetes mellitus (DM).
 It occurs in patients with mild or occult DM and most of them are middle aged to
elderly. Underlying renal insufficiency or congestive heart failure is common and
their presence worsens the prognosis.
 Common precipitants for DKA are similar to those of DKA (see previous section)

Essentials for diagnosis:

 Plasma osmolality > 320 mosmol/kg.
 Arterial pH > 7.30.
 Serum HCO3 > 15 mmol/L
 Level of consciousness: stupor/coma.

Differential diagnosis:
1- Diabetic ketoacidosis.
2- Hypoglycemic coma.
3- Stroke.
4- Myocardial infarction.

Precipitating factor:
1- Acute infection : pneumonia, urinary tract infection.
2- CVA.
3- Myocordial infarction.
4- Acute pancreatitis.
5- Intestinal obstruction.
6- Peritoneal dialysis.
7- Subdural Hematoma.
8- Thyrotoxicosis.
9- Cushing’s syndrome.
10- Acromegaly.
11- Drugs : β-Adrenergic blockers, calcium channel blockers, chloropromazine, diuretics
cimetidine, immunosuppressive drugs, corticosteroid and total parenteral nutrition.
12- Previously undiagnosed patients.

Clinical Presentation
 Polyuria and polydipsia
  Hypovolemia (tachycardia, hypotension, dry mucous membranes and poor skin
turgor)
 Lethargy and confusion progressing to convulsions and deep coma.

Diagnostic studies:
 Blood glucose
 Urea and electrolytes
 ABG
 CBC
 Urine general.
 ECG
 CXR
 Blood urine & culture.
 Brain CT (if stroke is suspected).

Goals of treatment:
- Improve circulatory volume and tissue perfusion.
- Decrease serum glucose and plasma osmolality towards normal levels.
- Correct electrolytes imbalance.
- Identify and treat precipitating factors.
- Education to prevent recurrence.

Treatment:
Preferably carried out at an ICU if feasible:

(A) IV Fluids:
 If patient in cardiogenic shock hemodynamic monitoring is needed.
 If patient is hypovolemic administer 0.9% NaCl (1) litre/hour and/or plasma
expander.
 Evaluate serum sodium : -
o If serum sodium is high i e > 150 mmol/L give 0.45 % NaCl at a rate of 4-14
ml/kg/hour depending on state of hydration.
o If serum sodium is lower or normal give 0.9% NaCl at a rate of 4-14
ml/kg/hour depending on the state of hydration.
 When serum glucose reaches 300 mg/dl change IV fluid to 5% dextrose in 0.45 NaCl
at a rate of 500 ml every four hours.

(B) IV insulin:
 Ensure that serum potassium level is satisfactory and follow the safety guidelines
given in the management protocol of DKA.
 Give soluble insulin of 0.15 units / kg/hour as IV bolus and continue with IV insulin
infusion at a rate of 0.1 units/kg/hour.
 Check serum glucose hourly and if serum glucose does not fall by at least 50mg/dl in
the first hour then double insulin dose hourly until glucose falls at a steady hourly rate
of 50-70 mg/dl.
  When serum glucose reaches 300 mg/dl change the replacement IV fluid to 5%
dextrose in 0.45% NaCl and decrease the infusion rate of intravenous insulin to 0.05-
0.1 units/kg/hour to maintain serum glucose between 250 mg/dl to 300 mg/dl until
plasma osmolality is < 315 mosmol/kg and patient is fully alert.
 After recovery from HHS subcutaneous insulin can be resumed on the same
guidelines given in the treatment of DKA.

(C) IV potassium chloride

 Follow the same guidelines given in DKA.

(D) IV heparin: -
 Can be given as heparin infusion of 1000 units/hour.
 Observe closely for any bleeding.
 Monitor APTT every (8) hours.
(E) Treatment of underlying condition.

Complications of treatment:
 Hypoglycemia.
 Hypo & hyperkalaemia.
 Pulmonary edema.
 Cerebral edema.
 Renal failure.
 Adult respiratory syndrome
 Systemic thromboembolism

Notes:

Hyperosmolar Nonketotic Coma

Flow Sheet Setup

Time Vital Urine Glucose K Intravenous Insulin

Signs Outpu Fluids
t
 Diabetic Lactic Acidosis

Lactic acidosis should be suspected in acidotic, hyperventilating diabetic patient who has a
high anion gap metabolic acidosis not accounted for by ketones, salicyltes, uremia or
methanol.
A lactate level of > 5 mmol/L is arbitrarily considered diagnostic.

Management:
 Take blood for CBC, glucose, urea, electrolytes ABG, serum and urine ketone , blood
lactate and urine general.

Correction of acidosis:
 Acidosis (PH < 7.1) has a negative inotropic effect, and persistent acidosis will lead
to shock & eventual death.
 If pH is below 7 give 2 mmol/kg body weight of sodium bicarbonate over the first
hour and then aliquots of 50 mmol over ½ hour to raise the plasma bicarbonate to 14
mmol/L over the next 24 hours.
 Ensure that ventilation is satisfactory by giving concentrated oxygen and observing
the blood gas series.
 Haemodialysis and peritoneal dialysis may be used.
 Prognosis is poor.
 Hypoglycemia
Definition:
Hypoglycemia is the clinical state resulting from low blood glucose, usually below 60 mg/dL.
It must be considered in any confused disorientated, aggressive or excitable person,
especially if they are known to be diabetic on insulin or taking sulphonylurea.

Common Precipitants:
 In diabetic patients:
o Excessive insulin and oral hypoglycemic agents (sulphonylureas)
o Missed meals
o Renal insufficiency.
 In non-diabetics:
o High insulin: exogenous insulin, sulphonyurea, insulinoma, anti-insulin or
insulin receptor antibodies
o Low glucose production: hypopituitarism, adrenal insufficiency, glucagons
deficiency, hepatic failure and alcoholism.
o Postprandial.

Clinical Presentation:
These are usually seen with serum glucose of 55 mg/dL or less:
 Central nervous system: irritability, tremulousness, visual disturbances, confusion, coma
or seizures. Autonomic nervous system: diaphoresis and palpitations.
 Occasionally hypoglycemia may present with focal neurological signs such as hemiplegia
or focal fits.

Management:
 Rapid bedside checking of blood glucose by glucometer rapidly distinguish between hypo
and hyperglycemic coma. However if you are in doubt give IV 50 ml of 50% dextrose. It
will do little harm to a patient in hyperglycaemic coma and will usually restore
consciousness in patients with hypoglycemic coma.
 Never give insulin as a diagnostic test for a diabetic patient who is in coma. In
hypoglycemia it is usually fatal and invariably disastrous
 If the patient can drink, give 25 gram dextrose in orange juice.
 If the patient is comatosed give 25 gram dextrose IV (50 ml of 50% dextrose) and when
the patient is awake a further 25 g to drink.
 Glucagon 1 mg IM can be given in patient whose hypoglycemia is proving difficult to
control with glucose infusions. Glucagons raises blood glucose to within the normal
range in 5-10 min, although its action is short lived.
 Recovery is usually complete in 10-15 min, but may occassionaly take up to 1 hour
despite adequate blood glucose levels.
 In case of delayed recovery from hypoglycemia coma consider the administration of IV
dexamethasone.
 If hypoglycemia attack is precipitated by sulphonylurea or longacting insulin it is
advisable to admit and observe the patient for 48 hours in order to avoid the danger of
recurrent hypoglycemia episodes over the next 24 – 48 hours
 Moreover, after the initial correction of hypoglycemia start your patient in 10% or 20%
dextrose drip over 24-48 hours to maintain blood glucose between 90-180 mg%.
 Thyroid Storm
Definition:
This is an extreme form of thyrotoxicosis manifested by marked delirium, severe tachycardia,
vomiting, diarrhea, dehydration and in many cases, high fever. The mortality is high.
Common precipitants are stressful illness, thyroid surgery, radioactive iodine administration
induction of anaesthesia, systemic illness (particularly infection or sepsis) or premature
discontinuation of antithyroid treatment in patients with hyperthyroidism..

Clinical Manifestations:
 Cardiovascular symptoms include tachycardia to rates that can exceed 140 beats/min,
along with congestive heart failure in many patients.
 Hyperpyrexia, agitation, delirium, psychosis, stupor, or coma are common and are
considered by many to be essential to the diagnosis.
 Severe nausea, vomiting, or diarrhea, and hepatic failure with jaundice can also occur.

Management:
 Admit the patient in an intensive care unit if feasible. Provide full hemodynamic and
respiratory support.
 Take blood for CBC, glucose, urea, electrolytes ,cortisol, T4 &T3 levels.
 Correct hyperpyrexia aggressively with a cooling fan, tepid sponging, paracetamol
and chlorpromasine 100 mg stat followed by 50 mg six hourly.. Avoid aspirin, which
can increase serum free (T4) and (T3) concentrations by interfering with protein
binding.
 Give propranolol by intravenous route, if available, in a dose of 0.5-2 mg every 4
hours. Concurrently, give propranolol orally or via nasogastric tube at a dose of 60 to
80 mg every four hours.
 Administer carbimazole (Neomercazole) 80 to 120 mg initially & then 20 mg six
hourly or propylthiouracil 800 to 1200 mg initially and then 200 mg every six hours
via nasogastric tube or rectally as necessary
 Propylthiouracil is the drug of preference because it also inhibits peripheral
conversion of T4 to T3.
 It is best to give the carbimazole or propylthiouracil 1 hour before giving the
potassium iodide , as this will ensure that the blockade of organification of iodine is
established before the potassium iodide is given.
 Potassium iodide (orally or IV) may also be administered to block the release of
thyroid hormone but this should not be used as the sole treatment preoperatively.
 The administration of potassium iodide without prior treatment with a thionamide
may exacerbate
 hyperthyroidism.
 Potassium iodide can be given as 200 mg IV over one hour and then 100 mg qds.
 High dose B-blockers should also be instiuted. Propanolol 2 to 5 mg IV every 4 hours
or 320 to 480 mg daily by mouth in divided doses to control heart rate.
 For hyperpyrexia: - fans can be used together with tepid sponges, paracetamol cooling
 Occasional patients have a severe associated myopathy that may lead to hypoxemia.
This may give rise to ventilatory failure. So monitor the arterial blood gas and be
prepared to institute intermittent positive pressure ventilatory support.
 Treat the underlying cause.
 Addisonian Crisis

Addisonian crisis may be:

 primary due to destruction and/or atrophy of the adrenal gland,or
 secondary due to failure of the hypothalamic-pituitary-adrenal axis.
The usual cause of secondary hypoadrenalism is the previous administration of exogenors
steroids.

Diagnosis:
 It should be considered in any hypotensive patient, who may also be vomiting,
especially if they have recieved steroids within the past year.
 It may be precipitated by infection, myocardial infarction,stroke, trauma,
surgery,parturition or any metabolic strees.
 It may complicate septicaemia caused by pyogenic organisms (such as the
meningococcus) and is said to be due to hemoarrhage into the adrenals.

Management:
 Take blood for baseline CBC, ABG ,electrolytes, urea, blood glucose and plasma
cortisol, urine general andCXR.
 If you suspect Addison’s disease, you should perform a short synacthen test before
giving any steroid replacement, so that you can retrospectively confirm your
diagnosis.
 Take a resting sample for cortisol analysis, then give 250 microgram of tetracosatrin
IV and take cortisol samples ½ and 1 hour later.
 However if tetracosatrin is not available do not delay management since that may cost
the patients life.
 Abdominal X-ray may show adrenal calcification.
 Steroid replacement : - give 100 mg of hydrocortisone IV followed by 50 mg IV
every 8 hours.
 Estimate blood glucose & if less than 2-3 mmol/L (40 mg/dl) give 25 grams of
glucose orally or IV.
 Start IV fluid preferably with CVP line and give at least one litre of normal saline in
the first hour, and then as necessary to keep the CVP within the normal range.
 If there is clinical evidence of sepsis start an IV broad spectrum antibiotics.
 Potassium supplement may be needed after initial resuscitation with normal
saline/glucose and IV glucocorticoids.
 Pituitary Apoplexy

Pituitary apoplexy occurs when sudden haemmorrhage and/or nercosis cause sudden
expansion of a pituitary tumor.

Diagnosis:
 Patient will present with a sudden onset of headache, visual impairment or loss, and
ophthalmoplgia.
 The patient becomes stuporous and may lapse into coma. Neck stiffness may be
present.
 CT scan or preferably MRI of the head may show pituitary hemoarrhage and
supraseller mass effect.
 Lumbar puncture is contraindicated because this presentation is consistant with
temporal lobe herniation.

Management:
 Request urgent neurosurgical consultation, since the relief of pressure by a transnasal
decompression is the procedure of choice.
 Gives dexamethasone 6 mg IV every six hours.
 Support circulation & ventilation.

Myxedema Coma

This represents the most severe extreme of hypothyroidism. The presence of stroke,
chloropromazine overdose and cold weather increases the susceptibility to this type of coma.
Before coma supervenes the patient may have been mentally dulled or psychotic.
Usually the patient has the classic appearance and signs of myxedema. Hypotension and
bradycardia are invariably present.

Management
 Measure blood glucose, CBC, urea, electrolytes, cortisol, T4 and T3.
 Hydrocortisone 100 mg IV stat & then 50 mg IV every 8 hours.
 Give thyroxine 300 to 500 micrograms IV bolus and then 100 mg IV daily thenafter.
The dose can be halved if you are confident that your patient is suffering from
ischemic heart disease.
 Continue with oral thyroxine as 100-200 micrograms OD thenafter.
 Monitor ventilation by blood gas assessment and supportive ventilation is needed in
most cases.
 For hypothermia use lots of blankets
 For hypoglycemia give 50ml of 50% dextrose as frequently as necessary.
 For hypotension it is advisable to monitor the central venous pressure and to use
inotrops to maintain the tissue perfusion and support the cardiac function.
 Provide glucose to avoid hypoglycemia.
 Treat the precipitating cause.
Gastro-intestinal
Emergencies
Editor: Amira Abbas Mohamed Fadl
 Acute Diarrhea In Adults
Definition:
Acute Diarrhea: is the passage of a greater number of loose form stools, than the normal,
lasting less than 14 days.
Diarrhea can be viewed as increase in the quantity of water and electrolytes in stools, leading
to a frequent production of unformed stools. It is the impaired balance between resorption
and secretion in the intestinal wall which leads to the increased wateriness of the faeces.

Pathogenesis:
 Non-invasive micro-organisms lead to diarrhea through a variety of interactions with
the intestinal mucosa. Enterotoxic E.coli and Vibrio cholerae do not spread beyond
intestinal lumen producing diarrhea through the production of enterotoxins which in
turn induce fluid secretion. Some micro-organism, such as Giardia lambelia, damage
the resorption surface of the microvilli, which in turn can lead to a disaccharidase
deficiency.
 Invasive micro-organisms penetrate the intestinal epithelium resulting in an
inflammatory disorder. The most well known example is that of Shigella infection.
Campylobacter and Salmonella too can invade the intestinal mucosa.

Causes

1-Bacterial 2-Viral 3-Parasitic 4-Non-

infectious
1. Sheiglla 1. Rotavirus 1. Gardia
2. Compylobacter 2. Norwalk 2. Entamoeba
jujeni virus 3. Cryptosoridium
3. Salmonella
species
4. E.Coli
5. Colisridium
difficili
6. Vibrio species

The transport vehicle of the common classic pathogens

Vehicle Classic Pathogen

Water Vibrio cholera, Norwalk virus, Giardia and
Cryptosporidium
Poultry Salmonella, Campylobacter and Shigella species
Beef E.Coli
Sea food Vibrio and Salmonella species.
Cheese Listeria species
Eggs Salmonella species
Cream Staphylococci, Salmonella and Clostridia.
Pies Salmonella, Campylobacter
Person to person Shigella, Cryptosporidium, Clostridium
(including sexual
contact)

Clinical Assessment:

Important Questions to Answer

1- Small bowel diarrhea or large bowel diarrhea?
2- Presence of fever?
3- Presence of blood?
4- Symptoms of nausea and vomiting?
5- Symptoms of abdominal pain?
6- Is there dehydration?
Note: Large volume diarrhea suggests small bowel origin. Usually it is unduly offensive and
contains large amount of fats.
Small volume diarrhea with tenismus suggests large bowel origin.

Assessment of Dehydration:
-Tachycardia -Dry tongue
-Postural drop of the blood pressure -Loss of skin elasticity

Possible risk factors for infectious diarrhea:

1- Recent travel especially to endemic areas.
2-Unusual food or eating habits.
3-HIV infection risks as in Homosexuals and IV drug abusers.
4-Recent use of antimicrobials, especially in the elderly and immunocoprommised.

Investigations:
1-CBC
2-Stool general
3-Stool culture
4-Toxins in stool: such as Colistridium deficile

5- Blood urea and electrolytes.

Management:
Rehydration:- using Oral Rehydration Solution (even when there is vomiting)
1. IV fluids for severe dehydrated cases.
2. Diet: Fasting is often not necessary, instead allow small meals.
3. Avoid milk and caffeine
4. Antdiarrheal medications: such as Loperamide are used for symptomatic treatment.
Avoid in Infectious diarrhea.
5. Antimicrobial: Not to be prescribed routinely. Most cases are self- limiting.
6. Consider using antimicrobials in (see table below):
a. Persistant bacterial and parasitic causes.
b. patients with artificial prostheses.
c. Immunocompromised patients.
 d. elderly patients.

Recommended Antimicrobial therapy

Organism Appropriate therapy (oral; adult dose)

Shigella Ciprofloxacin500mg bd-3/7
Salmonella Ciprofloxacin500mgbd-10/7; or Amoxicillin 750 mg 6hrly; 14/7
or Co-trimoxazole 960 mg BD; 14/7

Campylobacter Erythromycin 250 mg 6hrly; 5/7; or Clarithromycin 250 mg 6hrly;

5/7

Yersinia Doxycycline200mg day1, then 100mg daily; 4/7; or Co-

trimoxazole 960 mg BD; 5/7; or Ciprofloxacin 500 mg BD; 5/7

Amoebic Tinidazole 2g once daily; 3/7 ; or in dysentery: Metronidazole

750mg 8hrly; 5/7

Vibrio sp. Ciprofloxacin 1g once only ; or Vibramycin 300mg once only

Giardia sp. Tinidazole 2g once only

Strongyloides Albendazole 400 mg OD; 3/7 ; or ivermectine 150-200 ug/kg once

only

Cryptosporidium Paromycine500-1000 mg TDS; 14/7; or Azithromycin 500 mg

OD; 3/7

Clostridium Metronidazole 500 mg TDS; 10/7; or Vancomycin 125 mg 6hrly;

difficle 10/7

Cyclospora Co-trimexazole 960 mg TDS; 14/7

Trichuris Mebendazole 100mg BD; 3/7

Gastroenterology ‫ــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــ‬
Diarrhea workup algorithm: (Diarrhea < 3 weeks duration )
Acute diarrhea

Severe dehydration, fever, duration> 5dayes

Mucus or pus in BM, bloody diarrhea , abdominal pain, recent
Travel, or recent antibiotic use

Yes to any of the above No to all the above

Fecal leukocytes Observation

Occult blood Rehydration
as needed
C. Difficile toxin (esp. if recent a box

No fecal leukocytes + C. difficile toxin

fecal leukocytes of+
occult blood
Stool O&P X3
Pseudo
membranous colitis
-O & P -O & P Stool cultures
?flexible sigmoid scope Metronidazole PO or
(Vancomycine PO
for metronidazole
failure)

Medication- Include viral Stool Cultures Cx + fiex sig &BX

Enterotoxins, non-invasive
Bacteria.
Parasitic Invasive or cytotoxic
non-invasive Bacteria. IBD
Observation, Rehydration
?ABCs if symptoms severe
 Antiparastics Antiparastics
Eeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeee
0 Upper GIT Hemorrhage
Introduction:
Acute upper gastrointestinal bleeding is the commonest emergency managed by
gastroentrologists. It has an incidence ranging between 50 to 150 per 100 000 of the
population each year worldwide. In spite of the vast development in technical equipments as
endoscopes and improvements in medical and surgical expertise, the mortality remained
unchanged over the last few decades, which is about 10% in non-variceal bleeding and up to
30% in variceal bleeding. Mortality is reported to be lower in specialised units and this
probably because of adherence to guidelines and protocols.

Definitions :
o Hematemisis is vomiting fresh red blood .
o Coffee ground vomiting is vomiting of altered black blood .
o Melena is the passage of black tarry stools
o Hematochezia is passage of fresh blood coming from an upper GIT source.

Etiology:

Causes of acute upper gastrointestinal :

Diagnosis Approx %
Peptic ulcer 35-50
Gastrointestinal erosions 8-15
Esophagitis 5-15
Varices 5-10
Mallory Weiss tear 7-10
Upper gastrointestinal malignancy 1-3
Vascular malformation 3-5
No cause found Up to 20

Admission arrangements:
Patients with upper gastrointestinal bleeding should be admitted ideally to a specielised
gastrointestinal unit, which are usually jointly managed by medical and surgical staff. When
local circumstances do not permit this then they should be admitted to an acute general
medical ward where the staff have experience in managing such patients. Severely ill patients
are best admitted to a high dependency unit or intensive care unit.

Blood tests taken urgently at initial presentation

 Hemoglobin , platelet count , and white blood cell count
 Hematocrit.
 Urea, creatinine and electrolytes .
  Blood grouping and cross matching.
 Prothrombin time .

Assessment of bleeding severity:

It is essential to categorise patients at the time of admission into high or low risk of death.
Rockall et al defined independent risk factors (see table below) which were subsequently
shown to accurately predict death. These includes:

1. Increasing age: Death is rare in patients under 40 years of age but higher in patients aged
60 years and above, reaching 30% in patients aged more than 90years.
2. Comorbidity: The number and severity of comorbid illnesses are closely related to
mortality in patients admitted with GIT bleeding. Patients who have advanced liver or
renal disease and those with disseminated cancer fare worst. It is crucial that complicating
diseases affecting the heart, respiratory system and central nervous system are recognised
and appropriately managed
3. Shock: Defined as a pulse rate of more than 100 beats/min and systolic blood pressure of
less than 100mmHg.
4. Endoscopic findings: Normal upper GIT endoscopy, Mallory Weiss tear or the finding
of an ulcer with a clean base are associated with a low risk of rebleeding and death. In
contrast, active bleeding from a peptic ulcer in a shocked patient carried an 80% risk
risk of rebleeding in hospital.

Rockall scoring system for risk of rebleeding and death after admission to
hospital for acute gastrointestinal bleeding

Score
Variable 0 1 2 3
Age (y) <60 60-70 > 80

Shock No shock (systolic Tachycardia pulse > Tachycardia

BP>100, pulse<100) 100 Hypotension pulse >120
Systolic BP < 100 Hypotension
Systolic BP <80

Comorbidity Renal failure,

disseminated
malignancy
Diagnosis Mallory Weiss tear,
No lesion, and No
SRH
Major SRH None or dark spot

Cardiac failure,
ischemic heart
disease, Others
All other diagnoses Malignancy
upper
 GI tract
Blood in upper
GI tract, adherent
clot, visible or
spurting vessel
-2.
Each variable is scored and the total score calculated by simple addition . SRH: stigmata of
recent hemoarrhage.
For practicality it is important to classify patients with upper GIT bleeding on
admission into:

(1) Mild to Moderate bleed (2) Severe bleed.

This classification is especially relevant in the absence of immediate endoscopy

service.

1-Mild to moderate bleed:

 Age less than 60years.
 Pulse and blood pressure normal.
 Insignificant comorbidity.
 Hemoglobin concentration >10gm/dl.

2- Severe bleed:
 Age >60 years.
 Pulse > 100 beats/min .
 Systolic BP <100 mmHg.
 Hemoglobin < 10gm/dl.
 Significant medical diseases.

Management:
 Resusitation: The first and prime goal is to maitain oxygenation and to
restore blood volume.
 Intravenous access : Two large bore cannulae should be placed. In patients
with significant cardiac disease or patients with severe bleed a central venous
line (CVP LINE) is ideal for monitoring and replacement of fluids and blood.
(A clinical guide to management of hypovolaemic shock is shown in the table
below.)
 A urinary catheter to monitor hourly urine output.
 Patients with severe bleed are fasted until hemodynamically stable.
 Upper GIT Endoscopy within the first 24 hours of admission as it is:
o Diagnostic.
o Prognostic.
o Theraputic.
 Drug therapy three classes of drugs may be considered:
a. Acid suppressing drugs
i. An acidic environment makes a blood clot less stable. A pH > 6 is
necessary for platelets aggregation while a clot lysis occurs when the
pH falls < 6.
ii. Intravenous Proton pump inhibitors are superior to H2 blockers.
b. Somatostatin: High dose intravenous somatostatin has been shown to
suppresses acid secreation and reduces splanchnic blood flow, so it
works as an alternative haemostatic agent.
c. Antifibrinolytic drugs: Tranexmic acid therapy reduces the need for
surgical intervention and tends to reduce mortality in ulcer bleeding
patients.
 Surgery: The surgical team should be consulted early in the assessment of
patients with :(1)severe bleed (2)uncontrolled hemoarrhage by endoscopic
intervention (3)rebleed after an intial endoscopic control.
 Follow up:
o Patients who bled from ulcers should receive ulcer healing drugs plus
Hylicobacter pylori eradication if tested positive for it.
o Trials showed that eradication of H. pylori reduces the risk of recurrence
of ulcers and rebleeding.
o Ulcers associated with non-steroidals drugs (NSAIDs) should be given
proton pump inhibitors (PPI) for healing.If the need for NSAIDs continued
to be needed it should be covered by a PPI.
o Patients who bled from gastric ulcers should have a repeat endoscopy after
6 weeks to assess healing and exclude malignancy.
 Allgorithm for the management of acute gastrointestinal
hemoarrhage

Upper GIT bleeding

Routine blood tests + X match

Minor bleeding Major bleeding

Observation in general ward Active resuscitation in HDU/ ITU

Elective endoscopy setting
Early hospital discharge

Endoscopy
Varices No SRH

Major SRH See Varices Guidelines

Endoscopic therapy Observe in General ward

Successful Hemostasis Failure

Stable Rebleeding

Surgical operation

Consider H.pylori Repeat endoscopic

eradication and therapy Failure
PPI

Success

HDU : high dependency unit

PPI : Proton Pump Inhibitor
SRH : stigmata of recent hemoarrhage
 Treatment of Bleeding Esophageal Varices

Definitions:
Esophageal varices are portosystemic collaterals, i.e. vascular channels that link the portal venous
and the systemic venous circulation. They form with portal hypertension prefentially in the
submucosa of the lower esophagus (less often in gastric fundus, but varices may form in any
location along the GIT.

Pathogenesis:
Two important factors exist in the path physiology of portal hypertension, vascular resistance and
blood flow. Applying Ohm’s law P = F x R, where P= pressure gradient through the portal venous
system, F= volume of blood flowing through the portal venous system, R=resistance to flow.
Changes in either F or R affect the pressure.
A pressure difference between portal and systemic circulation (hepatic venous pressure gradient,
HVPG) of 12mm Hg is needed to form varices. Higher pressure increases risk of bleeding.

Mortality /Morbidity:
Variceal hemorrhage is the most common complication associated with portal hypertension.
Almost 90% of patients with cirrhosis develop varices and approximately 30% of varices bleed.
The first episode of variceal hemorrhage is estimated to carry a mortality rate of 30-50%, in spite
all the developments in medicine.

Common Causes of Portal Hypertension:

Prehepatic causes
 Portal vein thrombosis
 Splenic vein thrombosis

Intrahepatic (predominantly presinusoidal) causes:

 Schistosomiasis
 Primary biliary cirrhosis (early stage)

Intrahepatic: predominantly sinusoidal / post sinusoidal

 Hepatic Cirrhosis
 Primary biliary cirrhosis (advanced stage)
 Congenital hepatic fibrosis

Post hepatic:
 Inferior vena caval obstruction
 Budd-Chiari syndrome
Differential diagnosis:
Includes all causes of upper GIT bleeding. (see Upper G.I.T bleeding section)
It’s worth noting that peptic ulcer disease is common in cirrhotics. Thus, diagnosis requires
endoscopy

Treatment approaches:
Three different clinical situations have to be distinguished:
1- Treatment of acute variceal hemorrhag.
2- Prevention of a first variceal bleed (primary prophylaxis)
3- Prevention of re-bleeding after an initial bleeding episode (secondary prophylaxis)

Treatment of acute variceal hemorrhage

Resuscitation

o This is the prime step of management. It includes securing airway, giving oxygen,
stabilization of circulation. (ABC measures)
o Blood should be replaced at a modest target of Hematocrit of 25-30%.
o Avoid intravascular volume and variceal overexpansion to prevent rebleeding.
o Prevention of complications eg. hepatic encephalopathy, bronchial aspiration, renal
failure.
o It is important to monitor and correct electrolytes, urea/ creatinine, clotting profile, fluid
balance chart.
o All patients with cirrhosis and upper GIT bleeding are at high risk of developing severe
bacterial infections, which are associated with early re- bleeding.
o The use of prophylactic antibiotics has been demonstrated to decrease rate of bacterial
infections and increase survival rate. Broad-spectrum antibiotics such as ciprofloxacin and
3rd generation cephalosporins are used.

Pharmacological therapy
o Somatostain is an endogenous hormone that decreases portal blood flow by splanchnic
vasoconstriction, without significant systemic adverse effect.
o Octeriotide is a synthetic analogue of somatostatin. It is administered as a constant
infusion at 50 mcg/h.
o Vasopressin is most potent splanchnic vasoconstrictor. Its use is limited by systemic
vasoconstriction, especially of the coronary vessels. Continious infusion of 0.2-0.4 IU/min
is recommended.
o Vasopressin always should be accompanied by intravenous Nitro-glycerine at a dose of
40 mcg/min to maintain systolic blood pressure greater than 90 mmHg.
o Terlipressin is a synthetic analogue of vasopressin that has longer biological activity and
significantly fewer adverse effects than vasopressin.

Endoscopic therapy
o Has the advantage of allowing specific therapy at the time of diagnosis.
o Efficacy in achieving hemostasis is higher than 80%.
 o Failure of endoscopic treatments may be managed by a second session of endoscopic
treatment, but no more than 2 sessions should be allowed before deciding to perform Tran
jugular intrahepatic Porto systemic shunt (TIPS) or surgery.
o Endoscopic injection sclerotherapy involves injecting a sclerosant solution into the
bleeding varix, obliterating the lumen by thrombosis, or into the overlying submucosa,
producing inflammation followed by fibrosis.
o Sclerosant agents available are: 5% ethanolamine oleate and 1% to 3% sodium tetradecyl
sulphate. The typical volume used per injection is 2-5ml of sclerosant, with total volume
ranging from 20 to 30 ml.
o Complications of endoscopic injection sclerotherapy are related to the toxicity of the
sclerosant and include transient fever, stricture, perforation (rarely), chest pain,
mediastinitis, ulceration and pleural effusion.
o Endoscopic variceal ligation (EVL) is achieved by a banding device attached to the tip
of the endoscope. The varix is aspirated into the banding chamber, and a trip wire
dislodges a rubber band carried on the banding chamber, ligating the entrapped varix.
Leading to its thrombosis.
o EVL is less prone to complications than injection sclerotherapy.

Other interventions:
o Balloon-tube tamponade is used temporally in massive bleeding till a definite procedure
is done. Ideally an endotracheal tube should be placed to protect airways.
o Minnesota tube is a modification of Sengstaken-Blackmore (S-B) tube; the difference is
that the (S-B) tube does not have the esophageal suction port to prevent aspiration.
o The Minnesota tube has 4 lumens, 1 for gastric aspiration, 2 to inflate the gastric and
esophageal balloons and 1 above esophageal balloon for suction of secretions and prevent
aspiration.
o The tube is inserted through the mouth; its position within the stomach is checked by
auscultation while injecting air through the gastric lumen. Gastric balloon is inflated with
200 ml of air. Once fully inflated, use approximately 0.5 kg of traction, compressing the
submucosal varices. The esophageal balloon is rarely is required.
o Endoscopic administration of Cyanoacrylate monomer (superglue) in gastric varices is
another intervention.

Primary prophylaxis:
Primary prophylaxis is administered to patients at high risk of bleeding. These patients have (1)
large varices, red wale markings on the varices at endoscopy indicating thinning of varix wall due
to high wall tension or (2) severe liver failure as patients with Child-Pugh class B & C. (see table
1)

Beta-Blockers
o Beta-Blockers include Propranolol and Nadolol. They are non-cardioselective reducing
portal and collaterals blood flow. Reducing cardiac output and causing splanchnic
vasoconstriction.
o Propranolol is administered at a dose of 20mg every 12hrs, which is increased or
decreased every 3-4 days until a 25% reduction in the resting heart rate occurs or the heart
rate is down to 55 beats per minute. Average dose is 40mg bid.
o Nadolol dosing is half the daily dose of propranolol, administered once a day.
 o Propranolol is contraindicated in patients with asthma, chronic obstructive airway
disease, heart block, intermittant claudication and psychosis. Side effects (S/E) include:
fatigue, dyspnea on exertion, bronchospasm, insomnia, impotence and apathy. Reducing
dose usually helps with the S/E

Vasodilators
 Isosorbide mononitrate (ISMN) is a vasodilator and has been demonstrated to reduce
hepatic venous pressure gradient. Patient may develop tolerance to the drug.
 Available evidence does not support the use of ISMN as monotherapy, even in patients
with contraindications or intolerance to beta-blockers.
 Combination therapy involves both beta-blockers and ISMN. Unfortunately
associated with increased side effects.

Note:
 Prophylactic sclerotherapy has no role in primary prophylaxis.
 Prophylactic endoscopic variceal ligation has been shown to have an efficacy similar
to beta-blockers in prevention of first variceal bleed, but with increased adverse
effects.
 EVL may be an option for patients with large varices who have contraindication to or
cannot tolerate beta-blockers.

Secondary prophylaxis
 Nonselective beta-blockers are as effective as sclerotherapy in prevention of rebleed.
They reduce mortality as well. Doses are similar to those used in primary prophylaxis.
 Endoscopic sclerotherapy performed at weekly intervals. About 4-5 sessions are needed
for eradication of varices, which is achieved in nearly 70% of patients.
 Endoscopic variceal ligation (EVL) is associated with lower rebleeding rates and lower
frequency of esophageal strictures. Fewer sessions are needed for variceal eradication
compared with sclerotherapy.
 EVL is the treatment of choice. Sessions are done every 1-2 weeks intervals until variceal
obliteration (usually 2-4 sessions).
 Combination of EVL and pharmacological therapy: recent studies showed that EVL
plus nadolol plus sucralfate is more effective than EVL alone.

Surgical care:
Includes decompressive shunts, devascularization procedures and liver transplantation.
 Surgery has no role in primary prophylaxis.
 The role of surgery in acute variceal bleeding is limited in view of endoscopic therapy,
which control bleeding in up to 90% of patients.
 In those patients with failure of endoscopic therapy to control their bleeding TIPS is an
important option, as it is less invasive compared to surgery (see below).

TIPS: Transjugular Intrahepatic Porto systemic Shunt

Technique: under local anaesthesia with sedation via the internal jugular vein, the hepatic vein is
cannulated and a tract is created through the liver parenchyma from the hepatic to portal vein with
a needle. This is performed under ultrasonographic and fluoroscopic guidance. The tract is
dilated; an expandable metal stent is introduced, connecting hepatic and portal systems. Blood
from hypertensive portal vein and sinusoidal bed is shunted to the hepatic vein.

Indications:
1-Uncontrolled variceal bleeding, despite emergency endoscopic and/or pharmacological
treatment.
2- Recurrent variceal bleeding, despite adequate endoscopic treatment.
3-Isolated bleeding from fundal varices.
4-Bleeding portal gastropathy.
5-Budd Chiari syndrome.
6-Bleeding ectopic varices.
7-Refractory ascites.
8-Hepatorenal syndrome.
9-Protein loosing entropathy due to portal hypertension.

Causes of recurrent portal hypertension and bleeding after TIPS:

1- Stent dysfunction (as many as 50% of shunts may occlude in 1year) due to stenosis,
thrombosis, retraction or displacement.
2-persistant gastric varices associated with spontaneous splenorenal collaterals or associated with
massive splenomegaly.

Complication of TIPS related to technique:

1-neck hematoma, 2- cardiac arrhythmias, 3- perihepatic hematoma, 4- rupture of liver capsule, 5-
extra hepatic puncture of portal vein, 6-arterioportal fistula, and 7-portobiliary fistula.

Complication of TIPS related to porto-systemic shunting: 1- hepatic encephalopathy (occurs

in approximately 30%), 2- increased susceptibility to bactremia, and 3- liver failure.

Other complications: 1-TIPS associated hemolysis (approximately 10%) and 2- infection of

stent.
Drugs used in this section

Drug Main indication Recommended dose

Propranolol Prophylaxis of variceal 20mg every 12hrs, which is increased
bleeding or decreased every 3-4 days until a
25% reduction in the resting heart
rate occurs or the heart rate is down
to 55 beats per minute. Average dose
is 40mg bid.
Isosorbide Prophylaxis of variceal Regular tablet: 5-10 mg twice daily.
mononitrate bleeding Extended release tablet: Initial: 30-
60 mg given in morning as a single
dose; titrate upward as needed,
giving at least 3 days between
increases; maximum daily single
dose: 240 mg
Somatostatin Upper GI hemorrhage I.V. bolus: 25-50 mcg followed by
continuous I.V. infusion of 25-50
mcg/hour
Vasopressin Upper GI hemorrhage Continuous I.V. infusion: 0.5
milliunits/kg/hour (0.0005
unit/kg/hour); double dosage as
needed every 30 minutes to a
maximum of 10 milliunits/kg/hour
I.V.: Initial: 0.2-0.4 unit/minute,
then titrate dose as needed; if
bleeding stops, continue at same dose
for 12 hours, taper off over 24-48
hours.
Terlipressin Upper GI hemorrhage I.V.: Adults: 2 mg followed by 1 or 2
mg every 4 hours until bleeding is
controlled, for up to 36 hours

Table 1. Child-Pugh classification of cirrhosis

Variable Score: 1 point 2 points 3 points

Encephalopathy Absent Mild/ Moderate Severe/ Coma
Ascites Absent Slight Moderate
Serum Bilirubin (mg/dl) <2 2-3 >3
Serum Albumin (g/l) > 3.5 2.8- 3.5 < 2.8
Prothrombin time (seconds) 1-4 4-6 >6
If the total score is 5 or 6, the cirrhosis is class A; if the score is 7 to 9, the cirrhosis is class B, if
the score is 10 or higher the cirrhosis is class C. The prognosis is directly related to the score.

Appendix

If endoscopy is not readily available, one has to resort to pharmacotherapy in any suspected
variceal bleeding, i.e. in patients with hematemsis and signs of cirrhosis.
Pharmacotherapy might be applied:
1. As primary prophylaxis in a cirrhotic with signs of portal hypertension (splenomegaly,
thrombocytopenia) and/or impaired liver function tests.
2. As secondary prophylaxis in a cirrhotic with a history of upper GI bleed.

If pharmacotherapy is also not available and variceal bleeding is suspected, one must resort to
general resuscitation measures with the aid of balloon tamponade. The transfer of patient to an
institution where the necessary diagnostic/therapeutic means are available should then be
arranged.
 Bleeding esophageal varices

Oxygen
Securing airway
Resusitation Correction clotting
Restoring circulation
Monitoring urine

Start Terlipressin or Octeriotide

Plus IV antibiotics as 3rd generation cephalosporins

Arrange an emergency endoscopy

Band ligation

Confirm diagnosis Theraputic

Sclerotherapy

Bleeding controlled Uncontrolled

Tipss
Arrange for variceal eradication Rebleed
Plus non-selective B blockers
Surgical shunt
 Lower Gastrointestinal Bleeding

Definition:
Lower gastrointestinal bleeding is defined as bleeding occurring from a site below ligament of
Trietze.
The usual presentation is the passage of fresh, bright red blood per rectum.
Note: However, melena can occur from colonic bleeding(especially right side colon) and fresh
blood per rectum can occur from torrential upper gastrointestinal bleeding. It is therefore essential
to exclude upper GIT bleeding in such patients.

Causes:
The causes of lower GIT bleeding are essentially colonic. Common causes are:
1. Diverticular disease.
2. Andgiodysplasia.
3. Colorectal cancer.
4. Colonic polyps.
5. Infective colitis (such as chronic amoebic dysentery).
6. Inflammatary bowel dsease.
7. Ischemic colitis.
8. Small bowel lesions.
9. Hemorrhoides/piles.
10. Anal fissures.

Management:
1. Initial resuscitation is as for upper GIT bleeding.
2. Aim is to know site of bleeding:
 Proctoscopy( which is considered as part of clinical examination).
 Upper GIT endoscopy is done first(see above note.)
 Sigmoidoscopy. In about 10% of patients a lesion causing lower GIT bleeding is
encountered at sigmoidoscopy. If this is negative then proceed to:
 Colonoscopy. If this is negative or the bleeding is too brisk to detect the origin then
two options are there:
o Mesenteric angiography.Effective only if the bleeding is greaterthan 1-2 ml/min.
o Technetium scintiscan. It is very useful technique for localising site of bleeding (if
it is available).
 Following identification of the site of bleeding, the treatment may be through
 Endoscopic intervention (such as adrenaline injection and coagulation of bleeding
vascular lesion or polypectomy).
 Intervential radiology, as embolization of a bleeding vessel.
 Surgical.
Hepatic Encephalopathy and Fulminant Hepatic Failure (FHF)

Definitions:
1-Hepatic Encephalopathy:
A syndrome observed in patients with hepatic cirrhosis. It may occur in patients without cirrhosis,
who have undergone porto-caval shunt surgery.
An important prerequisite for the syndrome is diversion of portal blood into the systemic
circulation.
The syndrome is characterised by:
 Personality changes
 Intellectual impairment
 Depressed level of consciousness
2-Acute hepatic failure: Fulminant Hepatic Failure (FHF)
Hepatic encephalopathy developing in a previously normal liver, within 8 weeks of initial onset of
jaundice.
3-Sub-acute hepatic failure:
Hepatic encephalopathy developing 9-26 weeks after development of jaundice.

Pathogenesis:
The encephalopaty in FHF is due to increased permeability of the blood brain barrier and to
impaired osmoregulation within the brain. It is a common cause of death. The encephalopathy in
cirrhotics is due to neurotoxins as ammonia, GABA, mercaptans, false neurotransmitters as
tyramine and octopamine. Here rarely we get brain edema.

Causes of Fulminant Hepatic Failure

1-Viral hepatitis:
Hepatitis A, B, C, E, Delta agent , Hepes viruses , CMV, EB virus
2-Toxic substances and Drugs:
-Halothane -Valproic acid
-Isoniazid -Disulfiram
-Rifampicin -Mushroom poisoning
-Amine oxidase inhibitors -Some herbal medicines
-Carbon tetrachloride -Hydrocarbons
-NSAID’s -Acetaminophen
3-Ischemic liver necrosis:
-Wilson’s disease with intra- -Shock states.
vascular hemolysis -Autoimmune
-Acute Budd-Chiari syndrome hepatitis
-Congestive heart failure -Heat stroke
4-Acute steatosis syndromes:
-Reye’s syndrome -Dideoxyinosine
-Acute fatty liver of pregnancy -Neoplastic
-Tetracyclines
5-Malignant infiltration of the liver:
 -Lymphoreticular -Acute phase of CML
-Hodgkin’s and Non- -Metastatic liver disease
Hodgkin’s lymphoma (lung,breast,melanoma) AML

Diagnosis and investigation of FHF:

 Full Blood Count and Blood Group

 L.F.T.: Measure serum transaminases AST and ALT together with Albumin and
Bilirubin.
o In toxic or viral FHF, the serum transferases are significantly elevated due to
hepatocytes injury.
o In acute fatty and malignant infiltration the amino-
o transferases are moderately elevated.
 Hepatitis serology
 Clotting profile
 Random Blood Glucose
 Drug levels eg Paracetamol.
 S. copper and ceruloplasmin, 24hr urinary copper, when appropriate.
 Liver biopsy may be helpful, after correction of coagulopathy.
 CXR
 U/S abdomen and Doppler studies.
 Blood cultures and septic screen

Prognosis:
Depends on: (1) the ability of liver to regenerate (2) age of the patient (3) cause of the acute liver
failure (4) clinical course (5) occurrence of secondary complications and (6) duration and
severity of the coma.
Poor prognostic indicators are:
1- Prothrombin time greater than 100 seconds regardless of the stage of encephalopathy.
2- Presence of any three of the following:
a. Arterial pH <7.3
b. Age <10 or > 40 yrs.
c. Jaundice > 7 days before onset of encephalopathy.
d. Prothrombin time >50 seconds
e. Serum bilirubin > 18mg/dl.
Causes of death in FHF:
 Neurological complications as brain edema or intracranial bleed in 57%.
 Gastrointestinal hemoarrhage in 13%
 Bacterial infection and sepsis in 13%
 Hemodynamic complications in 8%
 Progressive respiratory and renal failure.
 Hypoglycemia and hypokalemia.
Management of FHF:
General:
 Intensive care nursing.
 Monitor vital signs, urine output, regular neurological and full physical examination.
 Monitor blood glucose, S.K+, FBC, Ur/Cr, Albumin and coagulation and correct
according to abnormality.
 Correct hypoglycemia with 10% up to 50%
 Dextrose, depending on its severity.
 Avoid intravenous saline give N- acetylcystine IV infusion if available.
Encephalopathy:
 Limit oral protein to 0.5-1 g/kg/day.
 Lactulose 20-30ml t.d.s.
 Avoid sedation
Bleeding:
 Avoid arterial puncture.
 Fresh Frozen Plasma FFP, if bleeding occurs.
 Ranitidine 50mg in 20ml over 2min t.d.s.,to reduce stress ulcers.
Renal impairment:
 Urea is falsely low in severe liver disease so creatinine should be measured.
 Correct hypovolemia.
 Avoid diuretics.
 Consider dopamine 2.5mcg/kg/min which is the renal dose.
 Hemofilteration or dialysis is indicated if serum potassium >6mmol, HCO3+ < 15mmol/l
or rising creatinine.
Infection:
 Meticulous care of IV lines and urinary catheter.
 Full septic screen including blood, urine and catheter cultures are taken before starting
antibiotics.
 Broad-spectrum antibiotics are recommended because patients are critically ill and
common signs of sepsis are often absent. IV Cefotaxime 1g twice daily is an appropriate
broad-spectrum antibiotic until culture results are available.
Cerebral edema:
 Occurs in 70-80% of patient with Grade 4 encephalopathy and is often fatal.
 Features include paroxysmal hypertension, dilated pupils, sustained ankle clonus.
 20% Mannitol 0.5g/kg I.V. over 10 minutes provided urine out-put is more than 30ml/hr.
Artificial hepatic support:
 Allows time for the massively damaged liver to regenerate and resume normal function.
 Many different methods have been tried, including exchange blood transfusions,
plasmapheresis.
Liver transplant:
 May be the only lifesaving procedure in FHF.
 In most centres worsening hepatic encephalopathy, clinical evidence of cerebral edema
and increasing prolongation of the prothrombin time after 24 to 48 hrs. of intensive
medical treatment are used as the key factors for recommending liver transplantation.
 The 1-year survival rate for such patients after liver transplant is 65%
Clinical Features of Hepatic Encephalopathy:
Grading of symptoms and signs of hepatic encephalopathy is as follows:
Grade 0:
 Minimal changes in memory, concentration, intellectual function and coordination.
Grade 1:
 Mild confusion, euphoria or depression
 Decreased attention.
 Slowing of ability to perform mental tasks.
 Irritability.
 Disordered sleep pattern, such as inverted sleep cycle.

Grade 2:
 Drowsiness, lethargy.
 Gross deficit in performing mental tasks.
 Personality changes, inappropriate behaviour.
 Disorientation to time.
Grade 3:
 Somnolent but arousable
 Unable to perform mental tasks.
 Disorientation about time and place.
 Marked confusion.
 Occasional fits of rage (aggressiveness)
 Incomprehensible speech.
Grade 4:
 Coma (with or without response to painful stimuli)

Other important physical signs:

 Fetor hepaticus
 Asterixis (Flapping tremor)
 Fever and other signs of infection
 Jaundice (may be minimal in early stages)
 Liver size (usually small in cirrhosis and acute hepatic necrosis)
 Spleen: usually normal size.
 Ascites: develops or increase.
 Venous hum.
 Rectal examination for melena.

Common Precipitants of Hepatic Encephalopathy in Liver Cirrhosis

1. G.I.T.bleeding: presence of blood in upper gastrointestinal tract results in increased
ammonia and nitrogen absorption from the gut.
2. Renal failure: this lead to decreased clearance of urea and other nitrogenous compounds.
3. Infection: may predispose to renal impairment and to increased tissue catabolism, both of
which increase blood ammonia level.
4. Constipation: increases intestinal production and absorption of ammonia.
5. Diuretic therapy: leads to hypokalemia and alkalosis both facilitate the conversion of
NH4+ to NH3+.
 6. Medications: drugs acting in C.N.S. such as opiates, benzodiazepines, antidepressants and
antipsychotic agents may worsen hepatic encephalopathy.
7. Dietary protein overload: an infrequent precipitating factor of hepatic encephalopathy.

Differential Diagnosis for Hepatic Encephalopathy

 Intracranial lesions: such as subdural hematoma, intracranial bleed, stroke, tumor.
 Infections: such as meningitis, encephalitis and intracranial abscess.
 Metabolic encephalopathy: such as hypoglycemia, electrolyte imbalance, hypoxia,
hypercapnia and uremia.
 Hyperammonemia from any other cause such as inherited urea cycle disorders or
secondary to uretrosigmoidostomy.
 Toxic encephalopathy from alcohol intake, such as acute intoxication, alcohol withdrawal
and Wernicke’s encephalopathy.
 Toxic encephalopathy from drugs such as sedative hypnotics, antidepressants,
antipsychotic agents and salycylates.
 Post-seizure encephalopathy.

Management of Hepatic Encephalopathy

The following steps showed be taken whenever possible:
 Precipitants of hepatic encephalopathy such as metabolic disturbances, gastrointestinal
bleeding, infection, sedative drugs and constipation should be corrected.
 Lactulose (beta-galactosidofructose) is a nonabsorbable disaccharide. It inhibit intestinal
ammonia production by a number of mechanisms:
1. Lactulose is degraded by colonic bacteria to lactic acid and other acids with
resulting acidification of intestinal lumen. This favors conversion of NH4+ to
NH3+ from tissues into gut lumen.
2. Gut lumen acidification inhibits ammoniogenic coliform bacteria.
3. Lactulose cause osmotic diarrhea, so reducing the stasis of bacterial load.
Dose: start with 30ml Lactulose (orally or by nasogastric tube) daily, twice or three times
daily. Aim for 3-4 loose motions per day.
S/E: diarrhea, abdominal cramps and bloating.(May consider reducing dose)
Lactulose may be given as enema to comatose patients.
Dose: 300ml Lactulose plus 700ml water administered as retension enema every 4 hours
as needed.
 Neomycin and other antibiotics such as: oral vacomycin, paromomycin, oral quinolones
and metronidazole are administered in an effort to reduce colonic ammoniogenic bacteria.
Neomycin is usually reserved as a second-line agent after lactulose.
Dose of Neomycin: 250mg orally 2-4 times /day. Doses as high as 4000mg /day may be
given. Long term treatment with this amino glycoside runs the risk of inducing ototoxicity
and nephrotoxicity because of some systemic absorption.
 Other drugs used in encephalopathy:
 L-ornithine L-aspartate (LOLA) stimulate urea cycle,where ammonia is used as a
substrate.This drug is new and found effective in a number of studies.
 Sodium benzoate interact with glycine to form hippurate. The subsequent renal excretion
of hippurate results in the loss of ammonia ions.Dose: 5g twice daily. S/E: sodium
retension, unpleasant taste.
 Diet: Rarely one should restrict proteins to less than 0.5g-1g/kg body weight in
encepalopathy.
 Vegetable proteins tolerated better than animal proteins, especially proteins derived from
red meat.!
 Mannitol: acts by reducing brain edema, mainly in culminant hepatic failure (FHF) rather
than in cirrhotics.(see pathogenesis above)
 Guidelines for Hepatic Encephalopathy
History
Signs

1. Sedative drugs 1. Conscious level

2. Gastrointestinal bleeding 2. Ascities
3. Fever with abdominal pain 3. PR for melaena/constipation
4. Constipation 4. Neurological examination to exclude
5. High-protein diet intracranial causes
6. Alcohol 5. Asterixis
7. Previous history of Acute or chronic 6. Fetor Hepaticus
liver disease 7. Jaundice and stigmata of chronic liver disease

Grading of Hepatic Encephalopthy

 Grade 0 Normal
 Grade 1 Euphoria or depression, abnormal sleep pattern, impaired
handwriting +/- asterixis
 Grade 2 drowsiness, grossly impaired calculation, asterixis
 Grade 3 Confusion, disorientation, somnolent but arousable, asterixis
 Grade 4 Stupor to deep coma unresponsive to painful stimuli

Investigation on Admission
1. FBC 2. SMAC 3. Blood glucose 4. Coagulation screen 5. Group & save 6. AFP
7. ABG’s if appropriate 8. X-ray chest 9. Infection screen 10. Abdominal paracentesis to exclude
spontaneous bacterial peritonitis 11. Abdominal ultra sound scan to exclude thrombosed portal vein
and hepatoma.

Treatment
1. Stabilise the patient ABC
2. Detection and correction of causes is a priority :-
 Gastrointestinal bleeding
 Infection (spontaneous bacterial peritonitis, other sites of sepsis)
 Hypokalaemia, metabolic acidosis
 High-protein diet
 Constipation
 Sedative drugs
 Uraemia after diuretic therapy
 Deterioration of liver function test
3. Fluid balance chart (avoid iv normal saline in patients with ALD)
4. Daily weight
5. Low salt diet
6. Protein restriction (or 0.5 gm/kg per day)
7. Lactulose 20 ml orally 2–4 times/day +/- phosphate enemas
8. Antibiotics (Neomycin 2-4 gm per day orally in divided doses OR Metronidazole 400 mg tds orally)
9. Supportive treatment :-
 Thiamine
 Multivitamins
 iv vit k 10mg (if coagulation is drained)
 reducing dose of chlordiazepoxide and prn dose
10. Monitor BM and treat hypoglycemia if present
Drugs used in this section

Drug Main indication Recommended dose

Lactulose Hepatic encephalopathy Oral: 20-30 g (30-45 mL) every 1-2 hours to
induce rapid laxation; adjust dosage daily
to produce 2-3 soft stools; doses of 30-45
mL may be given hourly to cause rapid
laxation, then reduce to recommended
dose; usual daily dose: 60-100 g (90-150
mL) daily
Neomycin Hepatic encephalopathy Oral: 500-2000 mg every 6-8 hours or 4-12
g/day divided every 4-6 hours for 5-6 days
Respiratory Emergencies
Editor: Ala’Eldin Hassan Ahmed
 Management of Acute Asthma Exacerbations in Adults
Definition:
Asthma is an inflammatory disorder of the airways associated with reversible airflow obstruction.
Airflow obstruction is assessed by measuring peak expiratory flow (PEF). Clinically asthma
presents as cough, and/or shortness of breath, and/or wheeziness and/or chest tightness. The
symptoms of asthma tend to be variable, intermittent, worse at night, and provoked by triggers
including exercise; these features are helpful in reaching a diagnosis.

Differential diagnosis:
 Congestive heart failure.
 Pulmonary embolism.
 Chronic obstructive pulmonary disease.
 Mechanical airway obstruction.
 Vocal cord dysfunction (rare).

Directed Approach to Acute Asthma Exacerbations:

History:
Determine how good or bad is the patient’s asthma control in the chronic stable state
 Symptoms especially the presence of nocturnal symptoms
 Range of home peak expiratory flow rates (PEFs), if available
 Frequency of emergency department visits and ICU admissions.
 Long-term medications including oral steroid dependence
Evaluate the following concerning the current exacerbation:
 duration
 severity (see next)
 potential precipitants
 medications taken in response

Physical examination:
 Asses asthma severity: Features of severe asthma are: PEF < 50% best or predicted;
respirations >/= 25/min; pulse rate >/= 110 beats/min; can’t complete sentences in one
breath.
 Features of life threatening asthma are: SpO2 < 92%; silent chest; cyanosis; poor
respiratory effort; bradycardia; arrhythmia; hypotension; exhaustion; confusion; coma.
 These findings are not sensitive indicators of severe attacks; up to 50 percent of patients
with severe airflow obstruction will not manifest many of these abnormalities.
 Look for signs of pneumothorax or pneumomediastinum.

Diagnostic studies:
1. PEF measurement:
 This is the best test for assessing the severity of an asthma attack.
  It is easy to perform and when repeated over time can be used to monitor a patient's
response to treatment.
 Predicted values for an individual differ with size, age, gender, and ethnicity, but a
peak flow rate below 200 L/min indicates severe obstruction for all but unusually
small adults.

2. Arterial blood gas (ABG) analysis:

 This is generally indicated only among patients with persistent dyspnea (despite initial
bronchodilator therapy) whose PEF is below 33 percent of predicted or those with
signs of life threatening asthma.

3. Chest x-ray:
 Generally not recommended for all patients.
 It can be limited to patients with suspected complications such as pneumothorax;
pneumomediastinum; consolidation; those with features of life threatening asthma; and
those who fail to respond to treatment satisfactorily.

For a stepwise approach for treating acute asthma exacerbations please refer to the
attached flowchart.

Notes:
 Give high flow oxygen to all patients with acute severe asthma.
 Ipratropium bromide provides greater bronchodilation for patients not rapidly
responding to initial beta agonist therapy.
 There is no evidence for any difference in efficacy between salbutamol and
terbutaline.
 Generally, avoid I.V. aminophylline if salbutamol is available. The combination of
salbutamol and intravenous aminophylline results in no further bronchodilation than
that achieved with nebulized beta agonists alone and may lead to increased risk of
toxicity.
 Rarely, however, some patients with near fatal asthma or life threatening asthma with
poor response to inhaled therapy may gain additional benefit from IV aminophylline 5
mg/kg loading dose over 20 minutes unless on maintenance oral therapy then give
infusion of 0.5 – 0.7 mg/kg/h.
 If PEF is < 50% on presentation prescribe prednisolone 40 – 50 mg/day. Continue
prednisolone 40 – 50 mg daily for at least five days or until recovery. This should be
followed by treatment with regular inhaled corticosteroids.
 In the absence of vomiting, oral administration of corticosteroids can be substituted for
intravenous administration. Oral formulations are rapidly absorbed and exhibit
comparable efficacy.
 If a nebulizer is unavailable, salbutamol may be delivered via a metered dose inhaler
(MDI) with a spacer. The equivalent dose has not been precisely defined, but four to
six carefully administered inhalations from an MDI with spacer have generally been
found to equal one nebulizer treatment.
 Routine prescription of antibiotics is not indicated for acute asthma.
Drugs used in this section:

Main Recommended dose

Drug indication
Prednisolone Acute  Oral: prednisolone 40 – 50 mg per day as single
asthma dose. Continue for at least five days or until
recovery
Hydrocortisone Acute  I.V. 100 mg 6 hourly is as effective as higher
asthma doses
Salbutamol (via Acute  Inhalation: 90 mcg/puff: 4 - 6 puffs every 20
a nebulizer OR asthma minutes for up to 4 hours, then every 1 - 4 hours
a metered dose as needed.
inhaler with a  Nebulization: 5 mg continuous flow nebulization
spacer) every 20 minutes for three doses. May also give
via continuous nebulization, at rate of 5-10
mg/hour.
Ipratropium Acute  Nebulization: 500 mcg 4 times/day.
bromide asthma  Metered dose inhaler: 2 inhalations 4 times/day,
Aminophylline Acute  I.V. loading dose (in patients not currently
asthma receiving oral aminophylline or theophylline): 5
mg/kg over 20 minutes (given in normal saline or
5% dextrose)
 I.V. maintenance dosage continuous infusions in
normal saline or dextrose 5%: 0.5 – 0.7
mg/kg/hour. Dosage should be adjusted according
to serum level measurement (if available)
Magnesium Acute  IV. 1.2 – 2 grams infusion in normal saline or 5%
sulphate asthma dextrose over 20 minutes (single dose)
 Algorithm of Management of Acute exacerpation of athma in adult in
emergency department
Measure Peak Expiratory Flow and Arterial Saturations

PEF>75% best or predicted PEF 33-75% best or predicted PEF < 33 & best or predicted
Mild Moderate - severe or any life threatening
features

Give usual bronchodilator Give salbutamol 5 mg by Obtain senior ICU help

oxygen driven nebulizer

High concentration oxygen

> 60%
Salbutamol 5 mg plus
ipratropium0.5 mg via
oxygen driven nebulizer
Clinically Clinically No life threatening Life threatening AND prednisolone 40 – 50
Stable and Stable and features features mg orally or IV
PEF>75% PEF<75% and PEF 50 –75% or PEF < 50%
hydrocortisone 100 mg

Repeat salbutamol 5 mg nebuliser. Measure arterial blood gases

Give prednisolone
40 – 50 mg orally Markers of severity
 PaOCO2 > 4.6 kPa
 PaO2 < 8 kPa
 Low pH

Give/repeat Salbutamol 5
Patient No signs of severe Signs of severe
mg plus ipratropium0.5 mg
recovering and asthma and PEF asthma or PEF <
PEF > 75% 50 -75% 50%
via oxygen driven nebulizer
after 15 minutes
Monitor SpO2,
Consider continous
heart and salbutamol nebuliser 5-10
respiratory rates mg/hr
Consider IV magnesium 1.2
– 2 grams over 20 minutes
Correct fluid/electrolytes
disturbances
Chest X ray
Patient stable and Signs of severe asthma
PEF > 50% or PEF < 50%

Potential discharge Admit ICU accompanied by

doctor
 Spontaneous pneumothorax
Definition:
Pneumothorax is defined as air in the pleural space. Primary pneumothoraces arise in otherwise
healthy people without lung disease. Secondary pneumothoraces arise in subjects with
underlying lung disease.

Differential diagnosis:
 Acute severe asthma.
 Acute pulmonary embolism.
 Acute left ventricular failure.
 Exacerbation of chronic obstructive pulmonary disease.
 Mechanical airway obstruction.

Directed Approach to spontaneous pneumothorax:

History:
There is no relationship between physical activity and onset of a pneumothorax; most pneumothraces occur at rest.
Smoking is a significant risk factor. Remember that history is not a reliable indicator of the size of a pneumothorax.

Physical examination:
 Look for signs of respiratory distress, cyanosis, and shock; if present they indicate
tension pneumothorax.

Diagnostic studies:
4. Chest radiograph. Expiratory CXR is not recommended for the routine diagnosis of a
pneumothorax.
5. A lateral chest or lateral decubitus radiograph should be performed if the clinical
suspicion is high but the PA film is normal.
6. CT scan is only recommended when differentiating a pneumothorax from complex
bullous lung disease.

N.B: For a stepwise approach for management of spontaneous pneumothorax (primary or

secondary) refer to flowchart.

Notes:
 If tension pneumothorax is present a cannula of adequate length should be promptly
inserted into the second intercostal space in the mid clavicular line and left in place
until a functioning intercostals tube can be positioned.
 The size of a pneumothorax is divided into small or large depending on the presence
of a visible rim of < 2 cm or >/= 2 cm between the lung margin and the chest wall.
 If a patient with a pneumothorax is admitted for observation, high flow oxygen (10
L/min) should be given.
 All breathless patients should not be left without intervention regardless of the size of
the pneumothorax.
 If > 2.5 L. of air were aspirated and the lung is not fully expanded (as indicated by
cessation of air coming out) the procedure should be abandoned and regarded
unsuccessful.
 There is no evidence that large tubes (20 – 24 F) are better than small tubes (10 – 14
F). The initial use of large tubes is not recommended.
 A bubbling chest tube should never be clamped or removed.
 If possible, pneumothorax patient should be admitted under the care of a respiratory
physician.
Recommended algorithm for the treatment of primary spontaneous
pneumothorax

Primary pneumothorax

No
Shortness of breath
and/or a rim of air > 2
cm on chest radiograph
Yes

Yes

Simple apiration
Successful ?
No

Yes

Consider repeat
Noaspiration
successful ?
Yes

Intercostal drain Remove 24 hours after

successful ? full expansion /
No cessation of air leak

Suction Consider
refer thoracic surgeon discharge
after 5 days
Recommended algorithm for the treatment of spontaneous secondary
pneumothorax

Secondary pneumothorax

No
Aspiration
Breathless + age > 50 successful ?
years + rim of air > 2
cm on chest radiograph
Yes No Yes

Admit to hospital
Yes
For 24 Hours
Intercostal drain
No
Successful ?

Yes Remove 24Yeshours after Consider

full re-expansion / discharge
cessation of air leak
NoSuction
successful ?

Discuss chest surgeon

After 3 days
 Management of Acute Pulmonary Embolism

Consider pulmonary embolism as a possible diagnosis in any patient presenting with acute
shortness of breath.

Differential diagnosis:
 Acute severe asthma.
 Acute left ventricular failure.
 Tension pneumothorax.
 Exacerbation of chronic obstructive pulmonary disease.
 Mechanical airway obstruction.

Directed Approach to Acute Pulmonary Embolism:

History:
Clinical presentation of pulmonary embolism may be subtle, atypical or obscured by other
coexisting diseases. In a patient with suspected pulmonary embolism determine the risks of
pulmonary embolism (see table)

Physical examination:
 Assess hemodynamic instability: low blood pressure or the presence of acute right heart
failure.
Diagnostic studies:
7. See figures

For a stepwise approach for diagnosing pulmonary embolism please refer to attached table
(rules for predicting the probability of embolism) and flowchart.

Notes:
 If the diagnosis of pulmonary embolism is strongly suspected, start treatment
immediately (before investigations are done or their results are available). See table:
drug treatment of acute pulmonary embolism for drugs used.
 Intravenous unfractionated heparin is as effective as low-molecular-weight heparin.
 For patients with severe renal failure unfractinated heparin is preferred over low-
molecular-weight heparin as low-molecular-weight heparin dose need to be monitored.
 Begin oral anticoagulation therapy within 24 hours of starting heparin.
 Discontinue heparin when the INR has been >/= 2 for two consecutive days.
 Thrombolytic therapy has not been shown to be superior to anticoagulation in the
management of pulmonary embolism.
 Thrombolytic therapy may be considered for patients who are hemodynamically
unstable.
Drug treatment of acute pulmonary embolism

Drug Main Recommended dose

indication
Unfractionate Acute Give bolus dose of 5000 units IV (or 80U/kg bolus).
d heparin pulmonary Followed by continuous infusion (in 5% dextrose or
embolism normal saline) of at least 30,000 units for the first 24
hours (18 U/kg/h.). Subsequent dosing should
maintain an aPTT value of 1.5 to 2.5 times the control
value.
Low Acute Can be used as an alternative to unfractionated
molecular pulmonary heparin. Body weight adjusted doses should be
weight embolism administered subcutaneously once or twice daily
heparin without laboratory monitoring. Follow
manufacturers’ recommendations for dosing.
Streptokinse Acute May be given to patients who are hemodynamically
pulmonary unstable (see text). Dose 250,000 units IV infusion
embolism ((in 5% dextrose or normal saline) over 30 minutes.
Should be followed by unfractionated heparin infusion
as above, or SC low molecular weight heparin as
above.
Warfarin Acute  Given orally as a single daily dose to maintain an
pulmonary INR between 2.0 to 3.0.
embolism
Rules for predicting the probability of embolism

Variable No of points

Risk factors
Clinical signs and symptoms of venous 3
thrombosis
An alternative diagnosis deemed less likely than 3
P.E.
Heart rate > 100 beats per minute 1.5

Immobilisation or surgery in the past 4 weeks 1.5

Previous deep vein thrombosis or P.E. 1.5

Hemoptysis 1

Cancer receiving treatment or treated past 6 1

months

Clinical probability
Low < 2.0
Intermediate 2.0 – 6.0
High > 6.0
Diagnostic Approach to a Patient with Low Clinical Probability
Pulmonary

Low clinical probability of embolism

CT angiography

Positive CT angiogram Negative CT angiogram

Diagnosis confirmed Duplex ultrasonography

Negative Positive

Diagnosis ruled out Diagnosis

confirmed
Diagnostic Approach to a Patient with High or Moderate Clinical
Probability of P.E

High or intermediate clinical probability of embolism

CT angiography

Positive CT angiogram Negative CT angiogram

Diagnosis confirmed Duplex ultrasonography

Negative Positive

Pulmonary Diagnosis
angiography confirmed

Negative Positive

Diagnosis Diagnosis
ruled out confirmed
Renal, Hypertensive and
Electrolyte Emergencies
Editor: Elwaleed Ali Mohamed Elhassan
 Acute Renal Failure

Definition:
Acute renal failure (ARF) is defined as a sudden decrease in renal function sufficient to increase
the concentration of nitrogenous wastes in the blood.
It is usually manifested by a rise in serum creatinine of, or more than, 0.5 mg/dl or 50% or a GFR
reduction by >50%.
In ARF, reduction of urine output is often seen:
 Oliguria, a decrease of urine output to less than 500 ml/day.
 Anuria is reduction of urine output to less than 100 ml/day.

Etiology:

Category Etiologies
Pre-renal  Hypovolemia, sepsis
(↓ renal blood flow)  Decreased effective arterial volume: heart failure,
cirrhosis (hepatorenal syndrome)
 Drugs: ACE inhibitors, NSAIDs, contrast dye,
cyclosporine
Renal  Acute tubular necrosis (ATN)
intrinsic renal o Ischemic: progression of any pre-renal process
pathology) o Toxins
o Drugs: aminoglycosides, amphoterecin, contrast
dye (usually only in setting of baseline renal
disease), pigments (myoglobin, Hb), crystals (uric
acid) or proteins (Ig light chains)
 Acute interstitial nephritis (AIN)
o Allergic: beta-lactam antibiotics, sulfa drugs,
NSAIDs
o Infection
o Infiltration (e.g. sarcoid, lymphoma)
o Autoimmune disease (e.g. SLE)
 Vascular: renal artery stenosis (esp. bilateral + ACE
inhibitors), thrombosis, hypertensive crisis, scleroderma
renal crisis, cholesterol emboli, HUS/TTP
 Acute glomerulonephritis (AGN)
Post- renal  Bladder neck: BPH, prostate cancer, neuropathies,
(obstruction of anticholinergic drugs
urine)  Ureteral: malignancy, lymphadenopathy, retroperitoneal
fibrosis
 Tubular: precipitation of crystals
Clinical presentation:
 Patients may present with non-specific symptoms due to azotemia and the underlying cause of
acute renal failure.
 Azotemia can cause malaise, nausea, vomiting, seizures, nonspecific abdominal pain and
platelet dysfunction which may lead to bleeding.
 Enquire about recent procedures and medications.
 Obtain vital signs, assess volume status. Look for signs of obstruction, pericardial effusion or
rub, vascular or systemic disease.
 Lung examination may reveal crackles due to fluid overload.
 Neurological examination may show altered sensorium and asterixis.

Workup:
1. Send blood samples for:
 BUN, s.creatinine, electrolytes including Ca and phosphorus. HCO³ and Chloride for
anion gap determination.
 CBC, uric acid and RBS.
 If diagnosis uncertain or clinical setting appropriate; obtain complement levels
(C3/C4), ANA, Anti DAN, ANCA, ASO titer, blood cultures and Bence Jones
proteins in urine
.

2. Evaluate Urine:
 Observe output.
 Get a sample for urinalysis, urine sediments, electrolytes and osmolality.
 Calculate the fractional excretion of Na (FE Na) = (Urine Na/Plasma Na) / (Urine
creatinine/Plasma creatinine):
1. Concentration ability preserved: urine osmolality >500 mOsm, specific gravity > 1.025,
decreased urine Na: < 20 meq/L, FE Na < 1% (e.g. pre-renal, contrast and pigment
nephrotoxicity, AGN, early post-renal)
2. Concentration ability impaired: urine osmolality <350 mOsm, specific gravity < 1.015,
decreased urine Na > 20 meq/L, FE Na > 1% (e.g. ATN, AIN, late pre-renal)

Etiology Sediment
Pre-renal Bland, few hyaline casts
Intrinsic
 ATN: pigmented granular casts
 AIN: WBCs and WBC casts; ± RBCs
 Vascular: bland, RBCs if necrosis
 AGN: Dysmorphic RBCs and RBC casts
Post-renal ± RBCs, WBCs, crystals

3. Renal ultrasound:
Is useful to rule out obstruction and evaluate kidney size to estimate chronicity of renal failure.
3. Renal biopsy: consider if suspect AGN or AIN
Treatment:
 Treat underlying disorder e.g. relieve obstruction if present, discontinue culprit medications.
 Optimize volume status:
o Give I.V crystalloids if suspected or established volume-depletion
o May start diuretics once fluid-replete to convert to nonoliguric state. Furosemide may
be administered intravenously (100-200 mg). If no favorable response, dose may be
repeated or doubled in 2 hours. It may be given in combination with metolazone. It
may also be given in a continuous I.V. infusion of 10-40 mg/hr (max 1000 mg/day).
o Support hemodynamics with pressors, inotropes if needed.
o Dialysis
 There are no specific proven treatments for reversal of ATN (i.e. no proven benefits for
dopamine, Furosemide or mannitol)
 Electrolytes disoders:
o Hyperkalemia:
 (See Hyperkalemia section)
 Decreased K intake, cation-exchange resin, dialysis
o Hyperphosphatemia: may use phosphates binders
 Correct drug doses for degree of renal insufficiency
 Fluid intake:
o After normal volume has been restored, restrict fluid intake to an amount equal urinary
and other losses plus insensible losses of 300-500 ml/day.
o In oliguric patients daily fluid intake may need to be restricted to less than 1 L/day.
 Nutritional support:
o High biologic value protein intake of 0.6 mg/kg/day.
o A daily diet comprising about 2 g of sodium, 40-60 mg of potassium and at least 35
kcal/kg of non-protein calories.
 Indications for urgent dialysis (when condition refractory to conventional treatment)
o Persistent severe academia with (pH less than 7.2)
o Life threatening electrolyte disturbances: e.g. hyperkalemia
o Intoxication: methanol, ethylene glycol
o Overload of volume unresponsive to diuresis
o Uremia: pericarditis, encephalopathy, seizures
Drugs used in this section:

Drug Main indication Recommended dose

Furosemide Augmenting diuresis in o I.V.: 100-200 mg/dose, may be repeated or
acute renal failure doubled in 1-2 hours as needed up to 1000
mg/day
o Continuous I.V. infusion: Initial I.V. bolus
dose of 0.1 mg/kg followed by continuous
I.V. infusion doses of 0.1 mg/kg/hour
doubled every 2 hours to a maximum of 0.4
mg/kg/hour if urine output is <1
mL/kg/hour have been found to be effective
and result in a lower daily requirement of
Furosemide than with intermittent dosing.
Metolazone Augmenting diuresis in Oral: 5-20 mg/dose every 24 hours.
acute renal failure
 Hypertensive Crises

Definition:
 Hypertensive crises are characterized by severe elevations in blood pressure (BP) with the
diastolic BP usually above 120 mmHg.
 They may be viewed as:
o Hypertensive emergencies, whereby there is evidence of ongoing end-organ
damage. Parentral treatment is usually needed.
o Hypertensive urgency, which is seen in the majority of patients, who have similar
BP elevations, but exhibit no such features. Oral therapy is employed

Hypertensive Emergency

This is defined by a significant elevation in BP associated with ongoing vascular damage

symptoms or signs of neurological, renal, cardiac or retinal dysfunction.

Hypertensive emergencies include severe hypertension in the following settings:

 Hypertensive encephalopathy (headache, irritability, and altered mental status due to
cerebral vasospasm).
 Malignant hypertension:
o Marked hypertension with new retinal hemorrhages, exudates, or papilledema.
o There may also be renal involvement, called malignant nephrosclosis and
manifests as hematuria, proteinuria and progressive renal dysfunction (by
comparing the presenting s. creatinine with a recent measurement) due to arteriolar
necrosis and intimal hyperplasia of the interlobular arteries.
 Aortic dissection
 Acute left ventricular failure and pulmonary edema.
 Unstable angina or acute myocardial infarction.
 Acute increase in sympathetic activity which can lead to severe hypertension in conditions
like: (1) pheochromocytoma; (2) autonomic dysfunction, as in the Guillain-Barré
syndrome; (3) renovascular disease (4) post-spinal cord injury
 Eclampsia and pre-eclampsia

Treatment
 Parentral treatment is usually indicated.
 Aim initially at rapidly lowering the diastolic BP to about 100 to 105 mmHg (or a
reduction in 25 percent of the presenting value, whichever is higher); this goal should be
achieved within two to six hours.
 Excessive reduction may precipitate coronary, cerebral or renal ischemia. Therefore agents
with a predictable, dose-dependant and transient effect are employed.
Best Practice Pharmacologic Management:

Nitroprusside sodium:
 Is the agent of choice in almost all hypertensive emergencies (except myocardial
ischemia, renal impairment or pregnancy)
 It is a combined arteiolar and venodilator reducing both afterload and preload.
 It is given as an intravenous infusion. Initial dose: 0.25 to 0.5 µg/kg per min; maximum
dose: 8 to 10 µg/kg per min. Nitroprusside acts within seconds and has duration of action
of only two to five minutes. Thus, hypotension can be easily reversed by temporarily
discontinuing the infusion, providing an advantage over the drugs listed below. However,
the potential for cyanide toxicity limits the prolonged use of nitroprusside, particularly in
patients with renal insufficiency. In most hospitals nitroprusside is only given in an ICU
with an arterial line in place.

Labetalol:
 An alpha- and beta-adrenergic blocker, given as an intravenous bolus or infusion.
 Bolus: 20 mg initially, followed by 20 to 80 mg every 10 minutes to a total dose of 300
mg. Infusion: 0.5 to 2 mg/min.

Nicardipine:
 A nondihydropyridine calcium channel blocker acting as an arteriolar dilator.
 Is given as an intravenous infusion. Initial dose: 5 mg/h; maximum dose: 15 mg/h

Enalaprilat:
 Is an angiotensin converting enzyme inhibitor and an ideal choice for patients with heart
failure.
 Is given as an intravenous bolus. Dose: 1.25 mg every six hours which might be increased
to 5 mg every six hours.

Alternative Drugs:

Hydralazine:
 Is a direct arteriolar dilator which causes reflex sympathetic stimulation of the heart.
Precautions are needed in patients with underlying coronary disease or an aortic
dissection, and a ß-blocker should be given concurrently to minimize the effect on the
heart.
 It is given in intravenous or intramuscular boluses. However, its effect is less predictable
than other agents.
 Initial dose: 10-20 mg/dose every 2-4 hours as needed. May increase to 40 mg/dose;
change to oral therapy as soon as possible.

Nitroglycerin
 Mainly is a venous dilator, given as an intravenous infusion. Is the drug of choice for
hypertensive emergencies with coronary ischemia.
 Disadvantages include being unstable in solution, tolerance with prolonged use and
profound headaches.
 Initial dose: 15 µg IV bolus, then 5-100 mcg/min (50 mg in 250 mL D5W); maximum
dose: 100 µg/min.
Hypertensive Urgency

Is severe asymptomatic elevation of blood pressure (systolic >220 Hg, or a diastolic >120 mmHg)
in the absence of indicators of acute end-organ damage.

Management:
 The initial goal should be a reduction in blood pressure to 160/110 over several hours with
conventional oral therapy.
 The simple combination of rest in a quiet room and an oral medication can lead to a fall in
BP to a safe level in many patients.

 The agent used should be effective, predictable, and unlikely to cause excessive
hypotension. Sublingual or oral fast-acting nifedipine is best avoided. Serious adverse
ischemic events have been reported in relation to its use.

 Best practice options include:

o Furosemide, 20 mg if renal function is normal and higher if renal insufficiency is
present.
o Labetalol, 200-400 mg, may be repeated every 2-3 hrs.
o Captopril, 12.5-25 mg every, may be repeated 1-2 hrs (because it is the ACE-I with
the shortest half-life)
o Felodipine, a long acting calcium channel blocker, 5 mg.

 Alternative:
o Amlodipine, 5 mg (less favorable option because of a rather delayed establishment
of action).

 Since almost all such patients require therapy with at least two antihypertensive
medications consideration should be made to combining two drugs initially. A diuretic
with another drug is reasonable.

 This regimen should lower the blood pressure to a safe level over three to six hours. The
patient can then be discharged on a regimen of once-a-day medications, with a close
follow-up to ensure adequate treatment.
 Emergency Treatment of Hypertension (1)
See text for details

Severe hypertension (SBP >220, DBP >120 mmhg)

?Does the patient exhibit symptoms or signs of ongoing end-organ damage

Hypertensive encephalopathy (headache, irritability, and altered mental

status)
Malignant hypertension:
Marked hypertension with new retinal hemorrhages, exudates, or
papilledema.
Malignant nephrosclosis (hematuria, proteinuria and progressive
renal dysfunction).
Aortic dissection
Acute left ventricular failure and pulmonary edema.
Unstable angina or acute myocardial infarction.

No Yes

Hypertensive urgency Hypertensive emergency

Aim to lower blood Proceed to intravenous

pressure to 160/110 therapy
over several hours with Lower the diastolic BP to
oral therapy about 100 to 105 mmHg or
The following options reduce by 25 % of the
may be employed: presenting value, whichever
is higher
Achieve this goal within two
to six hours.
Frusemide, 20 mg if renal function is
normal and higher if renal insufficiency is
present.
Labetalol, 200-400 mg, may be repeated
every 2-3 hrs. See next figure
Captopril, 12.5-25 mg every, may be
repeated 1-2 hrs
Felodipine, a long acting calcium
channel blocker, 5 mg.

Alternatively: Amlodipine, 5 mg
 Emergency Treatment of Hypertension (2)

Nitroprusside sodium:
Dose: 0.25 to 0.5
µg/kg per min; to a
maximum of 8 to 10
µg/kg per min.
Administer in an
Option for Intravenous ICU after an arterial
Drugs for Hypertensive
line is placed.
Emergencies

Labetalol:
Bolus: 20 mg
followed by 20 to
80 mg every 10
minutes to a total
of 300 mg.
Infusion: 0.5 to 2
mg/min.

Nicardipine:
Initial dose: 5 mg/h;
maximum dose: 15
Alternatives mg/h

Enalaprilat:
1.25 mg every six
hours; may
increase to 5 mg
every six hours.

:Nitroglycerin :Hydralazine
15 µg IV bolus, then 10-20 mg/dose every 2-4 hours
5-100 mcg/min (50 mg as needed.
in 250 mL D5W); May increase to 40 mg/dose;
maximum dose: 100 change to oral therapy as soon
µg/min. as possible.
Drugs used in this section:

Drug Main Indication Recommended Dose

Nitroprusside Hypertensive emergency Initial dose: 0.25 to 0.5 µg/kg per
sodium IV min; maximum dose: 8 to 10 µg/kg
infusion per min
Labetalol IV Hypertensive emergency Bolus: 20 mg initially, followed by
20 to 80 mg every 10 minutes to a
total dose of 300 mg. Infusion: 0.5
to 2 mg/min
Nicardipine Hypertensive emergency Initial dose: 5 mg/h; maximum
IV infusion dose: 15 mg/h IV infusion

Enalaprilat IV Hypertensive emergency 1.25 mg every six hours which

might be increased to 5 mg every
six hours
Hydralazine Hypertensive emergency Initial dose: 10-20 mg/dose every
2-4 hours as needed. May
increase to 40 mg/dose; change to
oral therapy as soon as possible
Nitroglycerin Hypertensive emergency 15 µg IV bolus, then 5-100
IV infusion mcg/min (50 mg in 250 mL D5W);
maximum dose: 100 µg/min
Furosemide Hypertensive urgency 20 mg if renal function is normal
PO and higher if renal insufficiency is
present
Labetalol Hypertensive urgency 200-400 mg, may be repeated
PO every 2-3 hrs.

Captopril PO Hypertensive urgency 12.5-25 mg every, may be

repeated 1-2 hrs
Felodipine, Hypertensive urgency 5 mg orally
Amlodipine Hypertensive urgency 5 mg orally
 Hypokalemia

Definition:
 Hypokalemia is defined by serum potassium (K+) less than 3.5 meq/L.

Etiology:
 The commonest cause of hypokalemia is loss of potassium from the gastrointestinal or
urinary systems when replacement is not adequate.
 However, hypokalemia can be transiently induced by the entry of potassium into the cells
(for example with severe hypoglycemia or salbutamol overdose).

Presentation:
 Muscular weakness, fatigue and muscle cramps are frequent complaints in mild to
moderate hypokalemia.
 Smooth muscle involvement may result in constipation or ileus. Flaccid paralysis,
hyporeflexia, tetany and rhabdomyolysis may be seen with severe hypokalemia. (<2.5
meq/L).
 The ECG shows decreased amplitude and broadening of T waves, prominent U waves,
premature ventricular complexes and depressed ST segments.

Workup:
 Rule out trans-cellular shifts: alkalemia, insulin, catecholamines, hypokalemic periodic
paralysis.
 Determine whether K+ depletion is due to gastro-intestinal (urine K+ < 15meq/L) or renal
(urine K+ >15 meq/L) losses. If renal losses, determine blood pressure and acid-base
status:

Gastro-intestinal (G.I) losses: (urine K+ < 25 meq/d or 15 meq/L)

 G.I. losses plus acidosis: diarrhea, laxative abuse, villous adenoma
 Vomiting and nasogastric tube drainage usually manifests as renal losses due to increased
aldosterone and metabolic alkalosis.
Renal losses: (urine K+ > 30 meq/d or 15 meq/L)
 Hypo- or normotensive:
o Acidosis: DKA, RTA
o Variable acid-base: Mg depletion
o Alkalosis: diuretics, vomiting, nasogastric drainage, Bartter’s syndrome.
Gitelman’s syndrome.
 Hypertensive
o Primary aldosteronism (Conn’s syndrome)
o Secondary aldosteronism (i.e. high renin states) renal artery stenosis, rennin
secreting tumors
 o Pseudohyperaldosteronism: licorice ingestion, Cushing’s syndrome, Liddle’s
syndrome.

Management:
 Optimal therapy is dependent upon the severity of the potassium deficit.

Evaluating the Potassium Deficit:

 The total potassium deficit in patients with hypokalemia due to potassium loss can only be
approximated, since there is no strict correlation between the plasma potassium
concentration and total body potassium stores.
 In general, the loss of 200 to 400 meq of potassium is required to lower the plasma
potassium concentration by 1.0 meq/L. Continued potassium losses below a serum level of
2 meq/L will not produce much more hypokalemia due to release of potassium from the
cell stores.

Potassium Replacement:
 An intravenous or oral potassium chloride preparation is generally preferred in the
treatment of hypokalemia.
 Oral replacement is safer because it is associated with less risk of hyperkalemia. A dose of
40 meq every 4-6 hours may be employed with frequent checking of serum K+.
 Use I.V. Potassium chloride should be reserved for patients:
o who are unable to eat
o who have severe or symptomatic hypokalemia
o whose GI tract absorption is impaired.
 In general, potassium can be safely given through a peripheral line in a concentration that
should not exceed 40 meq/L at rates of up to 10 meq/hr. A saline rather than a dextrose
solution is preferred for therapy as dextrose may promote potassium entry into cells
through stimulation of endogenous insulin release.
 If more rapid replacement is necessary, then 40 meq/hr can be administered through a
central venous catheter, but simultaneous ECG monitoring should be used.
 The underlying cause should be treated whenever possible, for example patients with
diuretic-induced hypokalemia may be re-evaluated for their need of diuretics or a
potassium-sparing diuretic might be added.
 Hypomagnesemia may lead to refractory hypokalemia. Patients with unexplained
hypokalemia or with diuretic-induced hypokalemia should have their magnesium checked
and repleted as necessary.
 Hyperkalemia
Definition:
 Hyperkalemia is defined as serum potassium (K +) of more than 5.5 meq/l in the absence of
hemolysis in the blood sample taken.

Etiology:
 The major causes of hyperkalemia are:
o Decreased excretion e.g. with renal insufficiency,
o Trans-cellular shifts as in metabolic acidosis,
o Hemolysis and rhabdomyolysis
o As an adverse effect of drugs (e.g. ACE-inhibitors, NSAIDs, spiranolactone and
cyclosporine.

Presentation:
 An elevated potassium (K+) concentration interferes with normal neuromuscular function
to produce muscle weakness and, rarely, flaccid paralysis. Abdominal distension and
diarrhea may occur.
 ECG is not a sensitive method for detection of hyperkalemia. However the first observed
change is peaking of the T waves (see figure) followed by flattening of P wave,
prolongation of PR then QRS intervals leading eventually to sine wave pattern.

Workup:
 Rule out trans-cellular shifts: acidosis, β-blockers, insulin deficiency (untreated insulin-
dependant diabetes), digoxin intoxication, massive cellular necrosis, hyperkalemic
periodic paralysis.
 Determine whether severely decreased GFR or normal GFR.
 If normal GFR determine why there is decreased effective aldosterone function.

 Decreased GFR:
o Any cause of oligo- or anuric renal failure or any cause of end stage renal disease

 Normal GFR (i.e. hypoaldosteronism)

o Hyporeninemic (i.e. type 4 renal tubular acidosis usually secondary to diabetic
nephropathy, ACE-inhibitors, NSAIDs)
 o Primary adrenal: Addison’s disease, congenital adrenal hyperplasia, heparin.
o Renal tubular disorders: K-sparing diuretics, cyclosporine, SLE, multiple myeloma,
amyloid

Treatment:

Treatment of hyperkalemia is divided into:

 Emergency interventions aimed at stabilizing the membranes and shift serum (K+) inside
the cells.
 Non-emergent, more definitive measures that decrease total body (K+) content.

The selection of the treatment approach depends on the clinical manifestations, the serum (K+)
level and the ECG changes:
 Plasma potassium concentrations above 7.0 meq/L or greater, severe muscle weakness, or
marked electrocardiographic changes are potentially life-threatening and require
emergency treatment.
 An asymptomatic patient with a plasma potassium concentration of 6.5 meq/L or less
whose ECG does not manifest signs of hyperkalemia can be treated only with a cation
exchange resin.
 Patients with a value below 6 meq/L can often be treated with a low potassium diet
and diuretics. In addition any potentiating drugs (such as nonsteroidal anti-
inflammatory drugs or angiotensin converting enzyme inhibitors) should be
discontinued.

For a stepwise approach for treating hyperkalemia please refer to the attached flowchart.
 Hyperkalemia (serum (K+)>5.5 meq/L in the absence of
hemolysis in the blood sample taken)
See text for details

Severe muscle Serum (K+) 7.0 meq/L or Marked ECG

weakness greater changes

Emergency treatment

Calcium NaHCO3, Regular insulin, 5-10 Nebulized salbutamol, 10-

Gluconate 44-88 meq units, plus dextrose 20 mg in 4 ml normal
10%, 5-30 ml (1-2 50%, 50 ml if saline, inhaled over 10
IV; or ampules) plasma glucose is < minutes
Calcium IV 250 mg/dl
Chloride 5%,
5-30 ml IV

Serum (K+) 6.5 or less Asymptomatic patient No ECG changes

Non-urgent treatment treatment

Frusemide, 40-160 Cation-exchange resin: Hemodialysis or

mg IV or orally Oral: 15-30 g in 20% sorbitol (50-100ml) Peritoneal
Rectal: 50 g in 20% sorbitol dialysis
 The following tables illustrate the different drugs used for treating hyperkalemia and their modes
of actions:

Emergent Treatment of Hyperkalemia

Modality Mechanism Onset Duration Prescription (K+)

of Action Removed
From Body
Calcium Antagonizes 0-5 1 hour Calcium Gluconate 0
cardiac minutes 10%, 5-30 ml IV; or
conduction Calcium Chloride
abnormailty 5%, 5-30 ml IV
Bicarbonate Distributes 15-30 1-2 hours NaHCO3, 44-88 meq 0
(K+)into cells minutes (1-2 ampules)IV
Insulin Distributes 15-60 4-6 hours Regular insulin, 5-10 0
(K+)into cells minutes units, plus dextrose
50%, 50 ml if plasma
glucose is < 250
mg/dl
Salbutamol Distributes 15-30 2-4 hours Nebulized 0
(K+)into cells minutes salbutamol, 10-20 mg
in 4 ml normal saline,
inhaled over 10
minutes

Non-emergent Treatment of Hyperkalemia

Modality Mechanism of Onset Prescription (K+)Removed

Action From Body
Loop Diuretic ↑ Renal (K+) 0.5-2 Furosemide, 40-160 mg IV Variable
excretion hours or orally
Sodium Ion exchange 1-3 Oral: 15-30 g in 20% 0.5-1 meq/g
Polystyrene resin binds (K+) hours sorbitol (50-100ml)
sulfonate Rectal: 50 g in 20%
(Kayxalate) sorbitol
Hemodialysis Extracorporeal 48 hours Blood flow ≥ 200-300 200-300 meq
(K+)removal ml/min. Dialysate [K+] ≈ 0
Peritoneal Peritoneal (K+) 48 hours Fast exchange 3-4 L/h 200-300 meq
Dialysis removal
 Hyponatremia

Definition:
Hyponatremia is defined by low serum sodium concentration (less than 130 meq/L) due to excess
water relative to sodium.
It is almost always due to excessive ADH secretion. This may either be:
 Appropriate: as in hypovolemia or hypervolemia but with decreased effective arterial
volume.
 Inappropriate: seen in the syndrome of inappropriate ADH secretion (SIADH).

Workup:
Determine serum osmolality (normal being 280-295 mosm/Kg H2O):
 Isotonic hyponatremia: a normal plasma osmolality is seen as a rare laboratory artifact due
to hyperlipidemia or hyperproteinemia.
 Hypertonic hyponatremia with a high osmolality is due to the presence of another
effective osmole (e.g. glucose or mannitol).
 Hypotonic hyponatremia: due to true excess of water relative to sodium. This is the case in
the majority of patients with hyponatremia.

Hypotonic Hyponatremia:
 Determine volume status (vital signs with orthostatic measurements, skin turgor, mucous
membranes, JVP, peripheral edema, urine output, BUN, Cr. and uric acid). Determine
whether hypovolemic, euvolemic or hypervolemic.
 Obtain urine Na concentration.
 Refer to figure for further diagnostic clues.

Treatment:

 Hypovolemic hyponatremia:
Volume replacement with isotonic (0.9%) saline.

 Hypervolemic hyponatremia:
Water restriction (1-1.5 L/d) and diuretics.

 Euvolemic Hyponatremia:

o Symptomatic:
Is usually seen with Na of <120 meq/L. If there are central nervous symptoms, hyponatremia
should be rapidly treated at any level of serum sodium concentration.

Rate of correction:
In chronic hyponatremia, brain cells secrete osmoles to minimize intracellular swelling. Too rapid
correction leads to raised serum osmolality in the setting of low brain osmolality. This results in
rapid water egress leading to acute brain demylination (central) pontine myelinosis.
However, acute symptomatic hyponatremia, especially associated with seizures or other
neurologic manifestations, and developing in less than 48 hours should be treated promptly as the
risk of brain edema far exceeds that of osmotic demyelination.
A reasonable approach is to increase the serum sodium concentration by no more than 1-2
meq/L/h and not more than 25-30 meq/L in the first two days; the rate should be reduced to 0.5-1
meq/L/h as soon as neurologic symptoms improve.
The initial goal is to achieve a serum sodium concentration of 125-130 meq/L, guarding against
overcorrection.

Hypertonic saline with Furosemide:

1. Calculate Na deficit that needs to be repleted to achieve Na of 120 meq/L:

Na deficit = 0.6 x ideal body weight x (120 – measured Na) (x 0.85 in females).
E.g. in a 70 kg man with a Na of 110 meq/L, must replete 0.6 x 70 x (120-110) = 420 meq of Na.

2. Calculate the number of liters of 3% saline (513 meq Na/L) needed to replete Na deficit, e.g.
to replete 420 meq of Na needs (420 meq Na)/ (513 meq Na/L) = 820 ml of 3% saline.
3. Calculate rate of infusion to achieve replacement at 1 meq/L/h e.g. to have serum sodium go
from 110 to 120 at a rate of 1 meq/L/h, infuse at 820 ml/10 hours = 82 ml/hr. Decrease the
infusion rate to 0.5 me/L/h as soon as neurologic symptoms improve.

These calculations are only approximation and careful follow-up of serum Na and infusion
adjustments are essential.

o Asymptomatic:
 In these cases the rate of correction need be no more than 0.5 meq/L/h.
 Water restriction, normal saline with Furosemide and demeclocycline may be employed.
 Demeclocycline (300-600 mg twice per day) is useful in patients who cannot adhere to
water restriction or need additional therapy. It inhibits the effect of ADH on the distal
tubule. Onset of action may require one week and concentration may be permanently
impaired.

Drugs used in this section:

Drug Main Indication Recommended Dose
Demeclocycline SIADH mg/day or 13-15 mg/kg/day 900-1200
divided every 6-8 hours initially, then
decrease to 600-900 mg/day
Hypertonic Hypotnic See text
saline 3% hyponatremia
 Hyponatremia algorithm

Serum osmolality

Normal Low High

(280-295 mosm/kg) (<280 mosm/kg) (>295 mosm/kg)

Isotonic Hypotonic Hypertonic

hyponatremia: hyponatremia hyponatremia:
hyperproteinemia, hyperglycemia, mannitol,
hyperlipidemia radiocontrast agents

Volume status

Hypovolemic Euvolmic Hypervolemic

Urine Na >20 Urine Na >20

SIADH
Postop hyponatremia
Hypothyroidism
Psychogenic CHF Renal
polydipsia Cirrhosis failure
Nephrotic
syndrome

Urine Na<10 Urine Na >20

Extra-renal losses: Renal losses:

Dehydration Diuretics
Diarrhea ACE inhibitors
Vomiting Nephropathies
Mineralocorticoid
deficiencies
Cerebral salt
wasting
 Hypernatremia

Definition:
 Is defined by high serum sodium concentration (> 145 meq/L) due to deficit of water
relative to sodium.
 It is almost always due to loss of hypotonic fluid and impaired access to free water (as
hypernatremia is a powerful thirst stimulus).

Workup:
 Check volume status (vital signs with orthostatic measurements, skin turgor, mucous
membranes, JVP, peripheral edema, urine output, BUN, Cr. and uric acid).
 Obtain urine sodium concentration and urine osmolality:
 If hypovolemic, determine whether renal (urine sodium>20 meq/L) or extra-renal (urine
sodium <10 meq/L) losses.
 If euvolemic, determine whether there is a lack of ADH activity (i.e. diabetes insipidus
with urine osmolality <300, but this usually presents with polyuria).
 Determine why patient is not drinking.
 Refer to figure for further diagnostic clues.

Treatment:
Rate of correction:
 In chronic hypernatremia, brain cells generate osmoles to minimize intracellular
dehydration. Too rapid correction leads to decreased serum osmolality in setting of high
brain osmolality. This may lead to rapid water ingress and acute brain swelling.
 Therefore, rate of correction of Na should not exceed 0.5-1 meq/L/h.

Hypovolemic hypernatremia:
 Replace volume (based on clinical judgment) and replace free water deficit:
o Free water deficit = 0.6 x ideal body weight x [(measured Na/140) – 1] (x 0.85
in females)
 Usually administer ½ or ¼ normal saline to simultaneously provide volume and free
water.

Hypervolemic hypernatremia:
 Loop diuretics and dextrose 5% in water.

Diabetes insipidus (DI):

 Central DI: desmopressin (dDAVP), a long-acting vasopressin analog.
 Nephrogenic DI: treat underlying cause; salt restriction + thiazide diuretics (reduces
delivery of filtrate to diluting segments of kidney).

Notes:
Diabetes insipidus (DI):
Is the condition in which antidiuretic hormone (ADH) is either absent (central) or has no effect
(nephrogenic).
Causes:
 Central:
 CNS trauma, surgery, hemorrhage, infection, granulomas, tumor, idiopathic
 Nephrogenic:
 Drugs: lithium, amphotericin, demeclocycline
 Metabolic: hypercalcemia, severe hypokalemia
 Other: polycystic kidney disease, sickle cell disease, SjÖgren’s syndrome, sarcoid,
amyloid.
Clinical Manifestations:
If patient with DI have intact thirst mechanism and are otherwise well usually present with severe
polyuria and mild hypernatremia
Lab Tests:
Urine oslmaolaity <300 mOsm (complete) or 300-600 mOsm (partial), confirmed by water
deprivation test
 Hypernatremia

Determine volume status

Hypovolemic or euvolemic Hypervolemic

Water Loss Na retention

Urine osm <300 Urine osm 300-600 Urine osm >600

Exogenous NaCl
infusion
Mineralocorticoid
Complete Renal water Extra-renal excess
Diabetes losses: diuretics, water losses:
Insipidus osmotic diuresis: GI
(glucose Insensible
,mannitol) losses
Partial Diabetes
Insipidus
Reset osmostat
Drug used in this section:

Drug Main Indication Recommended Dose

Desmopressin Central diabetes  I.V., Subcutaneous: 2-4 mcg/day (0.5-1
insipidus mL) in 2 divided doses or 1/10 of the
maintenance intranasal dose
 Intranasal (100 mcg/mL nasal solution):
10-40 mcg/day (0.1-0.4 mL) divided 1-3
times/day; adjust morning and evening
doses separately for an adequate
diurnal rhythm of water turnover
 Oral: Initial: 0.05 mg twice daily; total
daily dose should be increased or
decreased as needed to obtain adequate
antidiuresis (range: 0.1-1.2 mg divided
2-3 times/day)
 Hypercalcemia

Definition:
 Hypercalcemia is defined as a serum calcium level above the normal range of 8.5-10.5
mg/dl (2.1-2.6 mmol/L).

Clinical Presentation:
 Constipation and polyuria are syptoms of hypercalcemia irrespective of ca use (see notes
below), they ususally occur if the serum calcium is >12 mg/dl and tend to be more severe
if hypercalcemia develops acutely.
 Stupor, coma and azotemia may develop in severe hypercalcemia. Ventricular
extrasystoles and idioventricualr rhythm may also develop and can be accentuated with
digitalis.
 The focus of the history and physical examination should be on the duration of the process
of hypercalcemia and evidence for a neoplasm.

Workup:
 Obtain blood samples for serum calcium, phosphorus and albumin. When a significant
elevation of serum calcium is seen, it must be interpreted in relation to the serum albumin
level. Serum phosphate may or may not be low depending on the cause.
 The ECG shows a shortened QT interval.
 If feasible, measuremnts of 24 hr urinary calcium, PTH and PTH-related protein help
distinguish between malignancy-associated hypercalcemia and hyperpathyroidism.

Best Practice Treatment Algorithm:

The most effective therapy depends mostly upon the cause of the hypercalcemia:
 Until the primary cause can be brought under control, renal excretion of calcium with
resultant decrease in serum calcium is promoted.
 For mild cases (s. calcium concentrations 11-12 mg/dL):
o Encourage oral hydration and eating a high-salt diet.
o Glucocorticoids can be used for granulomatous causes of hypercalcemia.
 Oral phosphate binders can also be considered, as long as serum phosphate
concentrations do not exceed 4 mg/dL
 Acute therapy of patients with more severe or symptomatic hypercalcemia, (i.e. ,s.
calcium concentrations exceeding 12 mg/dL) consists of a three-pronged approach:
1. Expand volume with isotonic saline at an initial rate of 200 to 300 ml/hr that is
then adjusted to maintain the urine output at 100 to 150 ml/hr. Give Furosemide to
patients who are, or who get fluid-overloaded on this regimen. Frequent checking
and repleting for electrolytes is needed if diuretics are employed.
2. Administer salmon calcitonin (4 IU/kg), remeasure s. calcium in several hours. If a
hypocalcemic response is noted, then the patient is calcitonin-sensitive and the
calcitonin can be repeated every six to 12 hours.
 3. Administer a bisphosphonate: zoledronic acid (4 mg IV over 15 minutes) or
pamidronate (60 to 90 mg over two hours. The bisphosphonates will be effective
by the second to fourth day, thereby maintaining control of the hypercalcemia.
 Follow-up therapy is aimed at preventing recurrence of hypercalcemia.
 Tumors may respond to chemotherapy or radiation therapy leading to resolution of the
hypercalcemia.
 Additional more aggressive measures are necessary in the rare patient with severe,
symptomatic hypercalcemia.
 Hemodialysis with little or no calcium in the dialysis fluid and peritoneal dialysis
(though it is slower) are both effective therapies for Hypercalcemia.
 Dialysis may be indicated in patients with severe malignancy-associated
hypercalcemia and renal insufficiency or heart failure, in whom hydration cannot be
safely administered

Notes:

Causes of Hypercalcemia:

Increased bone Increased intestinal calcium Miscellaneous

resorption absorption

 Primary and  Increased calcium intake  Chronic lithium intake

secondary o Renal failure (often with  Thiazide diuretics
hyperparathyroidism vitamin D  Pheochromocytoma
 Malignancy supplimentation)  Adrenal insuffeciency
 Hyperthyroidism o Milk-alkali syndrome  Rhabdomyolysis and
 Other: Paget’s  Hypervitaminosis D acute renal failure
disease, estrogens and o Enhanced intake of  Familial hypocalciuric
antiestrogens in vitamin D or metabolites hypercalcemia
metastatic breast o Chronic granulomatous  Immobilzation
cancer, diseases (e.g. sarcoidosis)
hypervitamiosis A, o Malignant lymphoma
retinoic acid o Acromegaly
 Emergency Treatment of Hypercalcemia (1)
See text for details

Serum calcium(s.Ca) above normal range (10.5 mg/dl , 2.6 mmol/L)?

Obtain blood samples for:

serum calcium
phosphorus
albumin
interpret s.Ca in relation to the serum albumin levels:
Corrected s. Ca= measured Ca + [0.8(4–s.albumin)]
Get an ECG: may show shortened QT intervals

Confirmed hypercalcemia?

Obtain samples for:

24 hr urinary calcium
PTH and PTH-related protein

S. Calcium concentrations 11-12 mg/dL S. Calcium concentrations >12 mg/dL

Encourage oral hydration and eating a

high-salt diet proceed to next figure
May use glucocorticoids
hypercalcemia due to granulomatous
disease
May use oral phosphate binders as
long as serum phosphate
concentrations do not exceed 4
mg/dL
 Emergency Treatment of Hypercalcemia (2)
See text for details

S. Calcium concentrations >12 mg/dL

Expand volume with Administer Administer:

isotonic saline (NS) salmon calcitonin (4 zoledronic acid
at an initial rate of IU/kg) (4 mg IV over
200 to 300 ml/hr Remeasure s. 15 minutes)
Adjust NS infusion to calcium in several Or
maintain the urine hours pamidronate
output at 100 to 150 If a hypocalcemic (60 to 90 mg
ml/hr response is noted over two
Give frusemide to may repeate hours)
patients who are, or calcitonin every six
who get fluid- to 12 hours
overloaded on this
regimen
If diuretic employed,
frequently check and
replete electrolytes
Keep checking s. Ca
frequently.
If persistent or recurring
hypercalcemia consider
the following:

Chemotherapy or Hemodialysis with little or no

radiation therapy for calcium in the dialysate
malignant Peritoneal dialysis
hypercalcemia

Consider early dialysis in patients

with severe malignancy-
associated hypercalcemia and
renal or heart failure, in whom
hydration cannot be safely
administered
 Drugs used in treatment of hypercalcemia:

Drug Main indication Recommended dose

Calcitonin Severe or symptomatic I.M., Sub-Q: Initial: 4 units/kg every 12 hours;
hypercalcemia may increase up to 8 units/kg every 12 hours to a
maximum of every 6 hours
Zoledronic acid Severe or symptomatic 4 mg (maximum) given as a single dose infused
hypercalcemia over no less than 15 minutes; patients should be
adequately hydrated prior to treatment
(restoring urine output to ~2 L/day). Monitor
serum calcium and wait at least 7 days before
considering retreatment. Dosage adjustment
may be needed in patients with decreased renal
function following treatment.
Pamidronate 60-90 mg, as a single dose, given as a slow
infusion over 2-24 hours; dose should be diluted
in 1000 mL 0.45% NaCl, 0.9% NaCl, or D5W
Neurologic Emergencies
Editor: Elwaleed Ali Mohamed Elhassan
 Stroke (Cerebrovascualr Accident)

Definition:
The following are the cardinal features of a stroke:
 Characteristically, there will be sudden onset of neurological deficit
 The patient often has history of hypertension, diabetes mellitus, valvular heart disease or
atherosclerosis.
 In young adult patients a positive family history or history of narcotic abuse is frequently
noted.
 Often there are distinctive neurological signs reflecting the region of the brain involved.

Stroke can be broadly divided into acute ischemic (thromboembolic) or hemorrhagic stroke.
Approximately 80 percent of strokes are due to ischemic cerebral infarction and 20 percent to
brain hemorrhage.

The following is the differential diagnosis for acute stroke:

 Migraine
 Head trauma
 Todd’s paralysis (a deficit occurring after a seizure episode)
 Systemic infection
 Toxic metabolic disturbances (hypoglycemia, acute renal or hepatic insufficiency, drug
intoxication)
 Conversion reaction

Management Steps:

History:
 Get history from the patient or a relative regarding the onset and progression of the event.
Sudden onset (occurring over minutes to a few hours) is characteristic.
 The presence of headache at the onset and vomiting favor the diagnosis of hemorrhagic
compared with a thromboembolic stroke while an abrupt onset of impaired cerebral
function without focal symptoms or signs favor the diagnosis of subarachnoid hemorrhage
(SAH).
 Ask whether the patient takes insulin or oral hypoglycemic agents, has history of a seizure
disorder or drug overdose or abuse. Enquire about medications on admission, or recent
trauma.
 Enquire about atherosclerotic risk factors or a relevant cardiac history.

Physical Examination:
 Ensure a patent airway and adequate respiration. Intubation may be necessary to restore
adequate ventilation and to protect the airway from aspiration, especially in the presence
 of vomiting, which occurs commonly with increased intracranial pressure (ICP). Check
the oxygen saturation and administer supplemental oxygen if patient is hypoxic.
 Look for signs of endocarditis, bleeding tendency, valvular cardiac lesions or irregular
rhythm.
 Examine the neck and retroorbital regions for vascular bruits. Examine the fundus for
papilledema or cholesterol emboli.
 Examine the head for trauma and tongue for lacerations that might indicate seizures.
 Perform a quick neurological examination to define the extent of the deficit.

Immediate Laboratory Studies:

 Electrocardiogram.
 Oxygen saturation if hypoxia is suspected. Chest radiography is indicated if lung or heart
disease is suspected.
 Chest radiography, urinalysis and blood cultures are indicated if fever is present.
 Blood samples for the following studies:
o Complete blood count including platelets and an ESR
o Electrolytes, urea nitrogen, creatinine (hyponatremia may present with focal
neurologic deficits)
o Finger stick and serum glucose as hypoglycemia can present with focal neurologic
deficits. This is important if patient is diabetic, taking insulin or oral hypoglycemic
medications.
o Prothrombin time and partial thromboplastin time
o Blood for type and cross match in case fresh frozen is needed to reverse a
coagulopathy if intracranial hemorrhage (ICH) is present
o Toxicology screen and blood alcohol level in selected patients.
o Consider evaluation for hypercoagulable state in young patients without apparent
stroke risk factors
 Emergent non-contrast brain CT is important in excluding cerebral hemorrhage. In the
acute stage a cerebral infarct will not show findings on non-contrast CT while a
hemorrhagic lesion will manifest with evidence of a lesion sometimes with mid-line shift.
If feasible, it should be obtained as soon as the patient is medically stabilized.
 In selected patients, a carotid duplex study, MRI and MR angiography may also be
necessary. Diffusion-weighted MRI is more sensitive than standard MRI in detecting
ischemia.

Management:
 Early treatment of a completed stroke (see note below for a brief classification of stroke)
consists of attention to general supportive measures. This includes ensuring a patent
airway and adequate respiration, caring for the sphincters and skin.

 Inserting a feeding tube may be hazardous and should be avoided in patients with altered
consciousness who may not be able to cooperate adequately with swallowing or indicate
inadvertent misplacement of the tube into the trachea.
Specific Best Practice Management for Acute Ischemic Stroke:

 I.V. thrombolytic therapy with recombinant tissue plasminogen activator (rt-PA) (0.9
mg/kg to a maximum of 90 mg, with 10% given as a bolus over 1 minute and the
remainder over 1 hour) is effective in reducing the neurological deficit in selected patients
when given within 3 hours.
 Prerequisites include:
o Lack of CT evidence of ICH
o Absence of certain contraindications.

 Blood pressure management:

Acute management of blood pressure (BP) may vary according to the type of stroke. An effort
should be made to determine the type of stroke based on history and CT scan.

Acute Ischemic (thromboembolic) Stroke:

 Lowering the BP in the acute phase should generally be avoided as there is loss of the
cerebral autoregulation. Lowering the BP may further compromise ischemic areas.
 High blood pressure should only be acutely treated if:
o Extreme elevation (diastolic BP above 120 mmHg and/or systolic BP above 220
mmHg)
o the patient has active ischemic coronary disease, heart failure, or aortic dissection
 In the absence of those conditions, antihypertensive therapy may be withheld for at least
10 days after a thromboembolic stroke

If pharmacologic therapy is given, intravenous labetalol is the drug of choice.

Acute hemorrhagic Stroke:

 Reducing the BP in patients with either intracranial (ICH) or subarachnoid hemorrhage
(SAH) may be beneficial by minimizing further bleeding and continued vascular damage.
However, it may adversely affect the cerebral perfusion pressure needed to counteract the
raised intracranial pressure caused by the bleed.
 With ICH, intravenous treatment should be given if the systolic pressure is above 170
mmHg. The goal is to maintain the systolic pressure between 140 and 160 mmHg and to
carefully monitor the patient for signs of cerebral hypoperfusion induced by the fall in
blood pressure.
 With SAH, in the absence of ICP measurement, antihypertensive therapy is often withheld
unless there is a severe elevation in blood pressure. see notes below

Best Practice Drug Treatment:

 Intravenous labetalol is the first drug of choice because of easy titration and limited effect
on cerebral vessels.
 Dose: I.V. bolus: 20 mg or 1-2 mg/kg whichever is lower, I.V. over 2 minutes, may give
40-80 mg at 10-minute intervals, up to 300 mg total dose
 I.V. infusion: Initial: 2 mg/minute; titrate to response up to 300 mg total dose.
Administration requires the use of an infusion pump.
Alternative Blood Pressure Medications:
 Please refer to “Hypertensive Crises” section.
 Sublingual nifedipine should be avoided as it may precipitously drop BP and extend
ischemia.

Other Treatments:
 Early systemic anticoagulation may be warranted for treatment of acute cardio-embolic
and large-artery ischemic strokes. However, this is controversial as there is insufficient
data to support acceptable efficacy and lack of significant bleeding complications. In the
selected patients who receive heparin in the acute stroke setting, a bolus is not
administered.
 For embolic stroke due to atrial fibrillation (AF):
o Heparin should not be used in patients with atrial fibrillations presenting with
acute ischemic stroke.
o Warfarin (goal INR 2.0 to 3.0) can be initiated as soon as the patient is medically
and neurologically stable.
o In patients with large infarcts and those with poorly controlled hypertension the
initiation of warfarin therapy should be delayed for two weeks because of the
potential risk of hemorrhagic transformation.
o Aspirin: aspirin may be administered until warfarin is therapeutic.

 In patients with ischemic stroke (without AF) aspirin therapy (160 to 325 mg/day) may be
given within 48 hours of stroke onset. The optimal dose of aspirin is uncertain; there is no
compelling evidence that any specific dose is more effective than another and fewer side
effects occur with lower doses.

 Aspirin, clopidogrel (75 mg/day), and the combination of extended release dipyridamole
and aspirin (25/200 mg twice daily) are all acceptable options. However, initial therapy
with aspirin is recommended.

Notes:
Definitions:
 A completed stroke is a neurological deficit referable to a vascular territory which has
reached its maximum.
 A stroke in evolution is a progressive neurological deficit that has not reached its
maximum yet.
 A transient ischemic attack (TIA) is a focal neurological deficit of acute onset that
resolves completely within 24 hours.
 Subarachnoid hemorrhage refers to bleeding into the subarachnoid space. It is usually
caused by rupture of an aneurysm or an arteriovenous malformation
o The morbidity and mortality in SAH is related to two processes;
 Recurrent bleeding: early surgery (clipping or endovascular therapy) is advocated
for low grade SAH on Hunt and Hess classification. This is best guided by a
cerebral angiogram to define the bleeding vessel.
  Vasospasm: this causes ischemia which is responsible for neurological deficits in
SAH. It is attenuated by the calcium channel blocker nimodipine which has a
preferential vasodilator effect on the cerebral vessels. It is routinely used in SAH;
the dose is 60 mg every 4 hours for 21 days, start therapy within 96 hours after the
bleed.

Table of drugs used in this section:

Drug Main indication Recommended dose

Labetalol Acute lowering I.V. bolus: 20 mg I.V. over 2 minutes, may
of blood give 40-80 mg at 10-minute intervals, up to
pressure in acute 300 mg total dose.
stroke when
indicated I.V. infusion: Initial: 2 mg/minute; titrate to
response up to 300 mg total dose.
Administration requires the use of an
infusion pump.
Alteplase Acute ischemic I.V.: Doses should be given within the first 3
(recombinant stroke hours of the onset of symptoms;
tissue recommended total dose: 0.9 mg/kg
plasminogen (maximum dose should not exceed 90 mg)
activator) infused over 60 minutes.

Load with 0.09 mg/kg (10% of the 0.9 mg/kg

dose) as an I.V. bolus over 1 minute,
followed by 0.81 mg/kg (90% of the 0.9
mg/kg dose) as a continuous infusion over 60
minutes. Heparin should not be started for
24 hours or more after starting alteplase for
stroke.
Warfarin Acute embolic Start 5-10 mg daily for 2 days. Adjust dose
stroke due to according to INR results; usual maintenance
atrial dose ranges from 2-10 mg daily
fibrillations
Aspirin Acute ischemic 160-325 mg/day, initiated within 48 hours
stroke (in patients who are not candidates for
thrombolytics and are not receiving systemic
anticoagulation.
Clopidogrel Acute ischemic 75 mg daily
stroke
Aspirin and Acute ischemic 25/200 twice daily
extended-release stroke
dipyridamole
Nimodipine Subarachnoid 60 mg every 4 hours for 21 days, start
hemorrhage therapy within 96 hours after the bleed.
 Approach to Suspected Stroke
)See text for details(

Immediate general assessment:

Assess ABCs, vital signs
Provide oxygen by nasal cannula if hypoxic
Obtain I.V. access; obtain blood samples
Heart monitor, antipyretics as needed, DVT prophylaxis and early physical therapy.

Immediate neurological assessment:

Review patient’s history
Try to classify stroke type based on onset, progression, extent of involvement,
relevant medical history.

Urgent studies:
Electrocardiogram.
Oxygen saturation
Chest radiography, urinalysis and blood cultures if fever is present.
Blood samples for CBC, ESR, electrolytes, urea nitrogen, creatinine, finger stick
and serum glucose, PT/INR and PTT, toxicology screen and blood alcohol level in
selected patients.

Relevant history & Emergent non-

contrast brain CT showing ICH or SAH?

No Yes

Probable acute ischemic stroke: Consult neurosurgery

Treat high BP only if:
Extremely elevated (DBP above 120
mmHg and/or SBP above 220 mmHg) Initiate action for acute
The patient has active ischemic hemorrhage:
Reverse any anticoagulants
coronary disease, heart failure, or
Reverse any bleeding
aortic dissection disorder
In the absence of those conditions, Monitor neurological
withhold antihypertensives. condition
Thrombolytic therapy if within 3 hour Treat hypertension in awake
window and no contraindications patients.
 Status Epilepticus
Definition:
 Status epilepticus refers to the occurrence of a single unremitting seizure or frequent
clinical seizures without an interim return to normal consciousness.
 Any type of seizures can present in status epilepticus but the most serious is tonic-clonic
status.
 It is a life-threatening emergency which can be complicated by rhabdomyolysis, lactic
acidosis, aspiration pneumonitis, neurogenic pulmonary edema, respiratory failure and
neuronal death.

Predisposing factors:
 Withdrawal syndromes associated with the discontinuation of anticonvulsants, alcohol,
barbiturates, or benzodiazepines.
 Acute structural insult (e.g., encephalitis, cerebral malaria, stroke, head trauma,
subarachnoid hemorrhage, cerebral anoxia)
 Remote or longstanding structural injury (e.g., prior head injury, cerebral palsy, previous
neurosurgery, perinatal cerebral ischemia, arteriovenous malformations)
 Metabolic abnormalities (e.g., hypoglycemia, hepatic encephalopathy, uremia, pyridoxine
deficiency, hyponatremia, hyperglycemia, hypocalcemia, hypomagnesemia)
 Use of, or overdose with drugs that lower the seizure threshold (e.g., theophylline, high
dose penicillin G, quinolone antibiotics, metronidazole, isoniazid and cyclosporine).

Management Steps

Assessment and support:

 Promptly assess the patient with particular attention to respiratory and circulatory status,
offer supportive therapy (e.g., oxygen, mechanical ventilation) as needed.
 Treat hyperthermia promptly with passive cooling. It occurs relatively frequently during
status epilepticus and in many cases is primarily a manifestation of the seizures rather than
evidence of infection.
 Perform a rapid neurologic examination to provide a preliminary classification of the type
of status epilepticus and its probable etiology.
 Insert IV catheters, give 50 ml of 50% glucose and start a saline drip.
 Obtain blood for electrolyte, serum glucose, blood film for malaria, toxicology studies,
CBC, and rapid finger-stick glucose.
 Frequent measurement of blood pressure (BP), and pulse oximetry should be instituted.
Cardiac monitoring is advisable.

Best Practice Initial pharmacologic therapy

 Lorazepam or Diazepam:
 Lorazepam: administer 4 mg I.V. dose slowly over 2-5 minutes; may repeat in 10-
15 minutes; usual maximum dose: 8 mg. The clinical advantage of lorazepam is a
 longer duration of action because of its less pronounced redistribution into adipose
tissue.
 Diazepam: 5-10 mg slowly over 2 minutes every 10-20 minutes, up to 30 mg in an
8-hour period.
 If IV route is not immediately accessible a rectal diazepam gel formulation may be
used, the dose is 0.2 mg/kg.
 Phenytoin:
 If seizures continue place a second intravenous catheter in order to begin a
concomitant phenytoin loading infusion. Phenytoin and benzodiazepines are
incompatible and will precipitate if infused through the same line.
 Start phenytoin infusion of 20 mg/kg at 50 mg/min. Flush the vein with normal
saline after the infusion to prevent irritation.
 It is imperative to connect the patient to a cardiac monitor because hypotension
and serious arrhythmias may occur with infusion. Their risk increase with higher
infusion rates, reduce the rate if significant adverse effects are seen.
 If a monitor is not available, keep checking the pulse and BP manually frequently.
 Although approved for I.M. use, I.M. administration is not recommended due to
erratic absorption and pain on injection.

Treatment of refractory seizures

 If seizures continue, infuse another 10 mg/kg of phenytoin, review metabolic
derangements from initial laboratory studies and treat appropriately.
 Intubate and ventilate patient; admit to intensive care unit.
 Electroencephalographic (EEG) monitor, pulse oximetry and arterial catheter for blood
pressure monitoring are desirable.
 A drug-induced coma in the ICU is employed; neuromuscular paralysis is not an
appropriate treatment.
 Further pharmacologic therapy at this point is based primarily upon the patient's
hemodynamic stability:

Hemodynamically stable patients:

 Phenobarbital:
 20 mg/kg by slow infusion with a pump or intermittent injections (90-120)
mg/dose every 5-10 minutes) to a maximum of 1 gm at a rate of 50 mg/minute
 If seizures continue, infuse another dose of 10 mg/kg of while paying careful
attention to the EEG and hemodynamic status.
 Almost all patients at this point will require vasopressor support (typically
phenylephrine or dopamine) as well as crystalloid infusions. If seizures not yet
controlled proceed to the following options.

Hemodynamically unstable patients:

 Midazolam:
 0.2 mg/kg bolus, followed by a continuous infusion of 0.05 to 0.5 mg/kg per hour.
If this is unsuccessful within 45 to 60 minutes, a propofol infusion should be
started.
  Propofol:
 Loading dose 1-2 mg/kg followed by 2 mg/kg/hr, titrate to 10 mg/kg/hr. Adjust
dose to achieve seizure-free status on EEG.
 After seizures have been controlled for 12 hours, infusion of the anesthetic should
be slowly reduced and discontinued to allow for neurologic assessment. The drug
infusion should be resumed if epileptic activity is observed.

Long-term seizure control:

 A long acting anticonvulsant may be added once the status is controlled.
 Whenever feasible, dose adjustments are best determined by the clinical response and
serum drug levels.
 Best practice options for generalized tonic-clonic seizures:
 Phenytoin:
 Begin maintenance dose 12 hours after loading dose.
 Maintenance dose: 300 mg/day or 5-6 mg/kg/day in 3 divided doses or 1-2
divided doses using extended release tablets.
 If unable to swallow may give the same dose intravenously daily.
 Valproate:
 Initial: 10-15 mg/kg/day in 1-3 divided doses
 Increase by 5-10 mg/kg/day at weekly intervals until therapeutic levels are
achieved; maintenance: 30-60 mg/kg/day.
 Adult usual dose: 1000-2500 mg/day.
 Carbamazepine:
 200 mg twice daily to start
 Increase by 200 mg/day at weekly intervals until therapeutic levels
achieved
 Usual dose: 800-1200 mg/day in 3-4 divided doses; some patients have
required up to 1.6-2.4 g/day

 Alternatively:
 Phenobarbital:
 Oral, I.V.: 1-3 mg/kg/day in divided doses or 50-100 mg 2-3 times/day
 Initial Management of Status Epilepticus
See text for details

Assess and control airway

Monitor vital signs (including
temperature)
Conduct pulse oximetry and cardiac
monitor
Perform rapid blood glucose assay

Start intravenous infusion

Administer glucose (50 ml of 50 % dextrose)

Start anticonvulsant therapy

See next figure

Take focused history and examine patient Perform laboratory studies

 Known seizure disorder or other  CBC

illnesses?  Serum electrolytes and
 Trauma? calcium
 Focal neurologic signs?  Arterial blood gas if feasible
 Signs of medical illnesses? (e.g.  Liver function
infection, hepatic or renal disease ,  Renal function
substance abuse)?  Toxicology screen
 Serum antiepileptic-drug

Manage medical conditions

appropriately
 .1
mapezaroL VI :
nim/gm2 ta gk /gm1.0 mapezaiD
RO VI:
setunim 2 revo gm 01-5

Additional emergency drug may not be required if seizures

stop and the cause of status epilepticus is rapidly corrected

Seizures continuing

.2
ro )nim/gm
niotynehP
05 ta VI gk/gm 02(
)nim/gm
niotynehpsof
051 ta VI EP gk/gm 02(

Seizures continuing

.3

) gk/gm
niotynehP
01-5 lanoitidda(

Seizures continuing

.4

Phenobarbital (20 mg/kg)

IV at 50-75 mg/min

Seizures continuing

Proceed immediately to anesthesia with .5

midazolam or propofol if the patient is
hemodynamically unstable, has severe by Phenobarbital
systemic disturbances (e.g, extreme 01-5 lanoitiddA)
gk/gm (
hyperthermia) or has seizures that have
continued for more than 60 to 90 minutes
Seizures continuing
.6

htiw aisehtsen
A malozadim
lofoporp
ro

Time 80 70 60 50 40 30 20 10 0
(minutes)

Antiepileptic Drug Therapy for Status Epilepticus

See text for details
The horizontal bars indicate the approximate duration of drug infusions.
After N Engl J Med 1998; 338:970-976
Table of drugs used in this section:

Drug Main Indication Recommended Dose

Lorazepam Status epilepticus I.V.: 4 mg/dose given slowly over 2-5
minutes; may repeat in 10-15 minutes;
usual maximum dose: 8 mg
Diazepam Status epilepticus I.V.: 5-10 mg every 10-20 minutes, up to
30 mg in an 8-hour period; may repeat in
2-4 hours if necessary

Phenytoin Status epilepticus I.V.: Loading dose: 20 mg/kg;

maintenance dose: 300 mg/day or 5-6
mg/kg/day in 3 divided doses or 1-2
divided doses using extended release
Phenobarbital Status epilepticus Loading dose: I.V.: 300-800 mg initially
followed by 120-240 mg/dose at 20-minute
intervals until seizures are controlled or a
total dose of 1-2 g
Midazolam Status epilepticus I.V. bolus: 0.2 mg/kg followed by
continuous infusion at rates of 0.75 to 10
µg/kg per minute
Propofol Status epilepticus I.V.: 2 mg/kg over 10 minutes. If the
seizures stop prior to the infusion of the
entire bolus, the bolus should be
discontinued and a continuous infusion
begun at 4 to 12 mg/kg per hour. This
infusion should be titrated over the next
20 to 60 minutes to maintain a seizure-
free state and burst suppression on the
EEG.
Keep pressors at bedside and
continuously monitor BP and EEG.
Psychiatric Emergencies

Edited by: A.E.Abdelghani

 Psychiatric Emergencies
Problem-Based Approach

1. The violent aggressive patient

2. The suicidal patient

3. The unresponsive patient

4. Neuroleptic Malignant Syndrome

5. Other Neuroleptic Induced Problems

6. Medications Chart

Management of aggressive violent patients

Introduction

The threat of violence is an increasing concern in all branches of clinical medicine however the
out-patient clinics and emergency units in addition to psychiatric units and hospitals are areas of
high risk for violence (10% of patients in general psychiatric units have a history of violence).
The hostile patient may be actively violent, threatening violence, or have been violent. The aim is
to gain control of the situation quickly by an accurate assessment to ensure safety. The patient
should be offered or given the best available treatment.

Definitions
Violence is an act leading to physical injury or destruction to property.
• Aggression is any hostile or destructive behaviour or action directed towards others,
objects or self. It can be verbal, physical or sexual.

Presentation

 Acutely disturbed patient (excitement – agitation).

 Patient carrying weapons.
 Verbally aggressive and threatening patient.
 Physically aggressive patient.
 Escorted by police.
 Disinhibited patient.
Differential diagnosis

When dealing with hostile or violent patient, the most important task is to differentiate between
organic (physical) mental disturbances and functional psychiatric disorders.

A-Psychiatric / functional disorders

• Schizophrenia (especially paranoid type).
• Mania (excited states).
• Delusional disorders.
• Personality disorders: antisocial/ borderline / intermittent explosive.
• Depression (agitated).
• Post-traumatic stress disorder.
• A cute reaction to stress.
• Learning disabilities (mental retardation).

B-physical / organic causes

Violence may occur during delirious states or organic psychosis due to various physical causes:
1-systemic disorders
• Systemic infection.
• Hypoglycemia.
• Hepatic / renal impairment.
• Endocrine.
• Electrolyte imbalance.
• Intoxication (heavy metals, poisons etc).
2-Primary diseases of the brain
• Infection.
• Trauma.
• Epilepsy.
• Cerebro-vascular.
• Tumors.
• Dementia.
• Degenerative.
3- Drug intoxication / withdrawal
• Alcohol.
• Benzodiazepines.
• Amphetamines.
• Opioiods.
• Volatile substances (glue, benzene).
Assessment / work-up

• Take as many details as you can to make a quick assessment.

• Skilled multidisciplinay intervention can prevent or minimise violence.
• For a rapid screening the presence of any of the following is an indicator for:
Delirium
• Sudden onset.
• Cognitive impairment (impaired consciousness, disorientation).
• Hallucinations (visual / auditory).
• Known medical illness (DM, Hyptn).
Drug intoxication / withdrawal
• Physical signs of intoxication (smell of alcohol, glue, benzene, needle marks etc)
• Impairment of consciousness.
• Tremor, ataxic gait, pupillary changes, nystagmus, slurred speech.
• History of alcohol or drug abuse.
Schizophrenia / mania
• No impairment of consciousness.
• Intact orientation.
• Hallucinations.
• Delusions (paranoid/grandiosity).
• Thought disorder (disorganised, flight of ideas, etc).
• Mood disturbance (mania).
• Known psychiatric patient.

Personality disorders
• No impairment (of consciousness or orientation).
• No hallucinations or delusions.
• History of antisocial behaviour (aggression, stealing, frequent fights, drug abuse).
• History of impulsive behaviour.

Investigations

If possible:
• Quick physical examination
• Mental state examination
• Lab investigations to rule out life threatening medical illness: complete haemogram,
glucose, urinalysis, urea, electrolytes, LFT.
Other investigations: TFT, drugs and alcohol screening, ECG, CXR, EEG, lumbar puncture, CT,
MRI.
Management

When dealing with a violent patient, there are important points to consider:
• Safety of staff including yourself.
• Safety of the patient.
• Safety of the environment.
• Ethical, legal, and, cultural issues.

The best practice is the office:

• Should be properly equipped with solid furniture difficult to move, light chair for a shield,
and alarms.
• Should be spacious neither patient nor doctor should feel trapped and preferably with two
exits, but if one exit is available then the doctor should be near the door and staff should be
available for intervention.
Immediate management
Non-Pharmacological

Verbal diffusion

NO response

Phy sical control & restraint

No response

Seclusion
 Immediate management
Pharmacological
Haloperidol 5-10 mg i/m +
lorazepam2-4mg i/m Clopixol acqua phase
Or diazepam 10 mg i/v OR Chlorpromazine 50-100mg i/m OR 50-100mg i/m
Repeat af ter 2-3days
Wait f or 20 mins
No response

Repeat the dose

Wait f or 10-20 mins
No response

Continue until rapid tranqulization is achiev ed

OR Once “made saf e”
Up to a max. dose of 60mg haloperidol +60mg Exclude or treat underly ing cause
diazepam

Important notes:

1-Verbal diffusion (talking the patient down)

• Maintain adequate distance at least two meters away from patient, avoid corners.
• Identify yourself, be calm, confident and attentive, speak softly in non provocative way,
avoid intense eye contact, be neutral and concrete, and address the patient with respect using his
name.
• Hands should be kept in the midline avoid folded arms or having kept hands in hips or
pockets to avoid threatening gesture .Don’t turn away from the patient , turn sideways, move
backward if required.
• Engage in conversation, explain your intention, and acknowledge the patient’s concerns
and feelings.
• Listen to the patient, ask what is troubling him, help him talking about problems, reassure
avoid expressing contrary views at this stage avoid giving promises.
• Offer cold drinks if possible (avoid hot drinks).
• If the patient is armed, ask for weapon to be put down (not handed) and call for the police.

2-physical control and restraint

• Avoid force if possible and use minimum force and restraint necessary to prevent the
harm and release once the threat is over.
• Physical restraint should be used as a last resort.
• Secure adequate numbers of experienced staff trained in control and restrain techniques,
which approach the patient from behind, there should be one person for each limb and one for the
head the doctor administer the medications to immobilise the patient swiftly.
• Don’t slap, kick or punch, ensure cultural and gender sensitivity in addition to privacy and
dignity of the patient.

3-Seclusion
• This is a supervised confinement of a patient alone in a room which is locked for the
protection of others, from significant harm.
• Should be used as little as possible for the shortest possible time.
• Should not be used as punishment of the patient or convenience of the staff.
• Contra-indicated in delirious unstable or unknown medical status of the patient.
.

4-Rapid tranquilization
Refers to the process of calming or sedating the patient in order to create a safer environment
both for the patient and for others.
• Offer oral medications initially.
• Don’t give i/m diazepam use i/v route.
• Most patients respond in 20-40 mins.
• Reassess every 30 mins.
• In elderly or physically ill patients, give half doses.
• Monitor vital signs, check for possible respiratory depression, and dystonic reactions or
any other side effects of meds.
• Zuclopenthixol acqua phase has duration of action 2-3 days, should not be repeated until
after 48-72 hrs. Never give to psychotropic- naïve patient.
The suicidal Patient

Definitions

Suicidality
Refers to deliberate and potentially fatal acts of self harm.

Suicidal attempts and deliberate self harm (DSH)

A deliberate nonfatal acts whether physical, drug overdose, or poisoning done in the knowledge
that it was potentially harmful.
Any patients presents with suicidal attempt (DSH) or intention should be considered as
psychiatric emergency.

Presentation

 Patient with self inflicted physical injuries e.g., cutting hands or throat, hanging marks,
drug overdose…etc.
 Patient with depressed mood, psychomotor retardation, agitation, irritability,
worthlessness, hopelessness, guilt feelings, death wishes or communicating clear suicidal
intention
 Psychotic patient with nihilistic delusions, delusions of guilt or distressing auditory
hallucinations.
 Impulsive, emotionally unstable personality.

Differential Diagnosis

Suicidal attempts, intention or thoughts are usually part of depressive disorder but can arise in any
other psychiatric disorders. The most common causes:
 Depressive disorders
 Alcohol and drug abuse
 Psychotic disorders.
 Personality disorders.
 Chronic physical illness (pain, loss of limbs, terminal illness).

Management

The assessment and management of suicidal risk is one of the most fundamental tasks in
emergency psychiatry. When suspecting a suicidal risk immediate management involves the
following (see chart):
 Management of Suicidal Patient

Ensure that life saving measures are attended to first in cases of

bleeding wounds, poisoning, and drug overdose (physician/ surgeon)

Insure that medical / surgical teams are fully aware of the suicide
potential and that the patient is adequately supervised.

Involve and inform family members

When physically fit reassess suicidal intention and identify risk.

Treat agitation, anxiety and restlessness (Lorazepam 2 –4 mg)

Contact psychiatrist and transfer to psychiatric unit.

 The unresponsive patient (Stupor)

Definition

Psychological stupor is defined as mutism, immobility and no response to external stimuli,

without impairment of consciousness.
Stuporose patients usually display negativistic behaviour, refusing fluids and food intake which
endangers patient’s life and is considered as psychiatric emergency.

Presentation

It is important to differentiate psychological stupor (no impairment of consciousness) from

neurological stupor (medical emergency) which is characterized by impairment of consciousness.
The stuporose patient due to psychiatric disorder appears alert because of eye movements as if
awake but does not respond to stimuli. All vital signs are stable and there is no evidence of focal
neurological signs.

Differential diagnosis

Psychiatric
 Catatonia
 Depression
 Dissociative
 Manic

Organic
 Delirium
 Head injury
 Epilepsy
 Electrolyte and endocrine imbalance
 Space-occupying CNS lesions
 Drug induced

Management: see chart

 Management of the unresponsive patient (stuporous)

Ensure that there is no evidence of life-threatening acute brain syndrome.

Ensure that vital signs & neurological observations are stable
Exclude the possibility of drug-induced state or neuroleptic malignant syndrome.

Conduct full neurological examination, including; fundi, reflexes, pupillary size and
reaction to light. Check for muscular rigidity, neck rigidity or drug-induced
Parkinsonian symptoms.

Take samples for plasma glucose, urea, electrolytes, full blood count, & urine for
sugar, protein, & drug screen (if possible).

Neurological stupor Psychiatric stupor

Ask for CT brain, MRI, & EEG if Ensure adequate physical care; look for the
indicated. level of hydration, pressure sores, urinary
Obtain an urgent neurological retention, & concomitant physical illness.
opinion. Secure i.v line, insert urinary catheter, &
N/G tube.
Obtain urgent psychiatric opinion.
 Neuroleptic malignant syndrome (NMS)

Definition

This is a rare but potentially serious, even fatal neuroleptic-induced movement disorder which
represents a psychiatric emergency of mortality rate as high as 20% that can be reduced to less
than 5% with early recognition and intervention.

Presentation

Onset is acute, usually 2-28 days after taking neuroleptic drugs. The following are the essential
features:
 Hyperpyrexia
 Muscle rigidity, tremors, dysphagia
 Akinesea and mutism
 Clouded consciousness, confusion, coma
 Autonomic changes: tachycardia, increased respiration, elevated or labile BP, sweating,
pallor, and incontinence

Laboratory abnormalities

 Neutrophilia, raised CPK, raised K

 Altered liver enzymes
 Excess slow waves on EEG
 LP and MRI scan are negative

Differential diagnosis

 Infection
 Malignant hyperpyrexia
 Extra pyramidal disorder
 Lethal catatonia

Management: see chart

 Management of the neuroleptic malignant
syndrome (NMS)

If NMS is suspected (a patient on neuroleptics presenting with

the above features): Discontinue all neuroleptics immediately.

Treat secondary infection.

Bromocriptine up to 60mg daily.
Dantrolene up to 10mg/kg.
Sedation e.g, diazepam 10mg i.v.

 Cool the patient to reduce hyperpyrexia.

 Rehyderation
Monitor temp,&pulse,
electrolytes
BP. stabilization.
 Respiration, renal, & cardiovascular
Lab. Investigations as above. support.


 Contact a senior physician and make arrangements to transfer the

patient to acute care medical facility (if required).
 Contact a psychiatrist.
 Other neuroleptic-induced problems

Extrapyramidal side effects of neuroleptic drugs are common, although they are not life-
threatening, but are usually presenting to the emergency department because of their distressing
nature to both the patient and his family.

Acute dystonias
Can present as emergency because it can be painful and very frightening.
1. Occulogyric crisis: Muscle spasm causing eye rolling upwards.
2. Torticollis: Muscle spasm causing head and neck twisted to the side, the patient may be
unable to swallow or speak clearly. In extreme cases the back may arch (opisthotonous) or
jaw dislocates.

Management
Anticholinergic drugs given orally, i/m, or i/v depending on the severity.
1. Benzhexol 5-10mg.
2. Procyclidine 5-10mg.

Akathisia (restlessness)
This is a subjective unpleasant state of inner restlessness when there is a strong desire or
compulsion to move e.g. constantly pacing up and down, rocking, and foot stamping when seated.
Akthisia can be mistaken for psychotic agitation and has been linked with suicide and aggression.

Management
1. Reduce the antipsychotic dose.
2. Change to an atypical.
3. Propranolol 20-40mg/day.
4. Anticholinergics are generally unhelpful.

Drugs used in psychiatric emergencies

Medication Main Psych Indication Recommended Doses

Haloperidol Psychosis,excitement,aggression, 5-30mg/day
Agitation.
Chlorpromazine Psychosis,excitement,aggression, 200-1000mg/day
Agitation.
Zuclopenthixol Psychosis,excitement,aggression, 50-150mg/day
Agitation.
Diazepam Hypnotic, sedative, anxiolytic. 5-60mg/day

Lorazepam Hypnotic, sedative, anxiolytic. 2-6mg/day

Benzhexol Drug-Induced extrapyramidal symptoms 5-15mg/day

Procyclidine Drug-induced extrapyramidal symptoms 7.5-30mg/day
Dantrolene Muscle spasticity, malignant hyperthermia 25-400mg/day
Bromocriptine Neuroleptic malignant syndrome 10-60mg/day
Appendix 1
Malaria
 Appendix 2
List of Abbreviations Used in This Guidebook

Abbreviation Connotation
ABC Airway, breathing and circulation
ABG Arterial blood gas
ACE Angiotensin converting enzyme
ACE-I Angiotensin converting enzyme inhibitor
ACLS Advanced cardiac life support
ACS Acute coronary syndrome
AF Atrial fibrillations
AG Anion gap
AGN Acute glomerulonephritis
AIN Acute interstitial nephritis
ALT Amino alanine transferase
AML Acute myeloid leukemia
ANA Anti nuclear antibody
ANCA Antictyoplasmic antibody
ARF Acute renal failure
ASO Antistreptolysin antibody
AST Asparatate amino transferase
ATN Acute tubular necrosis
AVM Arteriovenous malformation
AXR Abdominal x ray
BD Twice daily
BP Blood pressure
BPH Benign proststic hypertrophy
BUN Blood urea nitrogen
CAD Coronary artery disease
CAP Community-acquired pneumonia
CBC Complete blood count
CCF Congestive cardiac failure
CCU Cardiac care unit
CHF Congestive heart failure
CK Creatinine kinase
CK MB Creatinine kinase, MB fraction
CML Chronic myeloid leukemia
COPD Chronic obstructive pulmonary disease
CPK Creatine phosphokinse
CSF Cerebrospinal fluid
CT Computerized tomography scan
CVA Cerebrovascular accident
CVP Central venous pressure
CXR Chest-X-ray
D5W Dextrose in water 5%
DBP Diastolic blood pressure
DI Diabetes insipidus
DKA Diabetic ketoacidosis
DM Diabetes mellitus
DSH Deliberate self harm
DVT Deep venous thrombosis
ECG Electrocardiogram
EEG Electroencephalogram
ESR Erythrocyte sedimentation rate
EVL Endoscopic variceal ligation
FHF Fulminant hepatic failure
GCS Glasgow coma scale
GFR Glomerular filtration rate
GI Gastrointestinal
Hb Hemoglobin
HDU High dependency unit
HUS Hemolytic uremic syndrome
IBD Inflammatory bowel disease
ICP Intracranial pressure
ICU Intensive care unit
ITU Intensive treatment unit
JVP Jugular venous pressure
LBBB Left bundle branch block
LDH Lactate dehydrogense
LFT Liver function tests
LMWH Low molecular weight heparin
LP Lumbar puncture
LRTI Lower respiratory tract infection
LV Left ventricle
LVH Left ventricular hypertrophy
MDI Metered dose inhaler
MI Myocardial infarction
MRI Magnetic resonance imaging
NMS Neuroleptic malignant syndrome
NSAID Non-steroidal anti-inflammatory drugs
NSTEMI Non-ST elevation myocardial infarction
O and P Ova and parasites
PAN Polyarteritis nodosa
PCWP Pulmonary capillary wedge pressure
PE Pulmonary embolism
PEFR Peak expiratory flow rate
PO Per orum (orally)
PPI Proton pump inhibitor
PRBC Packed red blood cells
PTH Parathyroid hormone
RBS Random blood sugar
RTA Renal tubular acidosis
rt-PA Recombinant tissue plasminogen activator
RVH Right ventricular hypertrophy
SAH Subarachnoid hemorrhage
SBP Systolic blood pressure
SIADH Syndrome of inappropriate ADH secretion
SIRS Systemic inflammatory response syndrome
SLE Systemic lupus erythematosus
SOB Shortness of breath
STEMI ST elevation myocardial infarction
SVR Systemic vascular resistance
TB Tuberculosis
TDS Thrice daily
TFT Thyroid function tests
TIA Transient ischemic attack
TIPS Transjugular intrahepatic porto-sytemic anastomosis
TMP-SMX Trimethoprim-sulfamethoxazole
TTP Thrombotic thrombocytopenic purpura
UA Unstable angina
URTI Upper respiratory tract infection
UTI Urinary tract infection
V/Q scan Ventilation-perfusion scan
VSD Ventricular septal defect
VT Ventricular tachycardia
 Appendix 3
Table of Drugs Used in This Guidebook

Drug Main indication Recommended dose

Acyclovir HSV encephalitis I.V.: 10 mg/kg/dose every 8 hours for 10-15 days
Alteplase Acute Coronary 15 mg IV bolus, then 0.75 mg/kg over 30 min(max
Syndrome 50 mg) then 0.5 mg/kg over 60 min (not to exceed
35 mg) (see section on Acute Coronary Syndrome)
Aminophylline Acute asthma I.V Loading dose (in patients not currently
receiving aminophylline or theophylline): 6 mg/kg
over 20-30 minutes; administration rate should
not exceed 25 mg/minute
Approximate I.V. maintenance dosages: Based
upon continuous infusions: smoker: 0.8
mg/kg/hour, nonsmoker: 0.5 mg/kg/hour, older
patients and patients with cor pulmonale: 0.3
mg/kg/hour, patients with congestive heart failure:
0.1-0.2 mg/kg/hour. Dosage should be adjusted
according to serum level measurement (if
available)
Amlodipine Hypertensive 5 mg orally
urgency
Amoxicillin Susceptible 875 mg every 12 hours or 500 mg every 8 hours
respiratory and
urinary tract
infections and
enteric fever
Amoxicillin Susceptible 875 mg every 12 hours or 500 mg every 8 hours
respiratory and
urinary tract
infections and
enteric fever
Aspirin Acute ischemic 160-325 mg/day, initiated within 48 hours (in
stroke patients who are not candidates for thrombolytics
and are not receiving systemic anticoagulation.
Aspirin Acute coronary ACS: Initial dose 300 mg (nonenteric formulation)
syndrome (ACS), followed by 100 mg/day.
acute ischemic AIS: 60-325 mg/day, initiated within 48 hours (in
stroke (AIS) patients who are not candidates for thrombolytics
and are not receiving systemic anticoagulation.
Aspirin and Acute ischemic 25/200 twice daily
extended-release stroke
dipyridamole
Benzhexol Drug-Induced 5-15mg/day
extrapyramidal
symptoms.
Benzylpenicillin Susceptible I.M., I.V.: 2-24 million units/day in divided doses
respiratory every 4 hours depending on sensitivity of the
infections and organism and severity of the infection
meningitis
Bromocriptine Neuroleptic 10-60mg/day
malignant
syndrome.
Calcitonin Severe or I.M., Sub-Q: Initial: 4 units/kg every 12 hours;
symptomatic may increase up to 8 units/kg every 12 hours to a
hypercalcemia maximum of every 6 hours
Calcium Chloride Emergency 5-30 ml IV
5%, treatment of
hyperkalemia
Calcium Gluconate Emergency 5-30 ml IV
10% treatment of
hyperkalemia
Ceftriaxone Urinary tract I.M., I.V.: 1-2 g every 8 hours
infection
Meningitis I.V.: 2 g every 12 hours
Cefuroxime Susceptible I.M., I.V.: 0.75-1.5 g every 8 hours (up to 1.5 g
respiratory every 6 hours in life-threatening infections)
infections
Chlorpromazine Psychosis, 200-1000mg/day
excitement,
aggression,
Agitation.
Ciprofloxacin Urinary tract Mild/moderate: oral 250 mg every 12 hours for 7-
infection and 14 days, I.V.: 200 mg every 12 hours for 7-14 days.
enteric fever Severe/complicated: oral 500 mg every 12 hours
for 7-14 days, I.V.: 400 mg every 12 hours for 7-14
days
Clarythromycin Susceptible Oral: 250-500 mg every 12 hours for 7-14 days
respiratory tract
infections
Clopidogrel (Plavix) Acute coronary 75 mg/d; for acute coronary syndrome, a loading
syndrome, acute dose of 4-8 tablets (300-600mg) can be used for
ischemic stroke rapid action.
(Use if ASA is
contraindicated)
Dantrolene Muscle spasticity, 25-400mg/day
malignant
hyperthermia.
Demeclocycline Syndrome of 900-1200 mg/day or 13-15 mg/kg/day divided
inappropriate every 6-8 hours initially, then decrease to 600-900
ADH secretion mg/day
Desmopressin Central diabetes I.V., Subcutaneous: 2-4 mcg/day (0.5-1 mL) in 2
insipidus divided doses or 1/10 of the maintenance
intranasal dose
 Intranasal (100 mcg/mL nasal solution): 10-40
mcg/day (0.1-0.4 mL) divided 1-3 times/day;
adjust morning and evening doses separately for
an adequate diurnal rhythm of water turnover
Oral: Initial: 0.05 mg twice daily; total daily dose
should be increased or decreased as needed to
obtain adequate antidiuresis (range: 0.1-1.2 mg
divided 2-3 times/day)
Diazepam Status epilepticus I.V.: 5-10 mg every 10-20 minutes, up to 30 mg in
an 8-hour period; may repeat in 2-4 hours if
necessary
Diazepam Hypnotic, 5-60mg/day
sedative,
anxiolytic.
Dopamine Hemodynamic I.V. infusion: 1-5 mcg/kg/minute up to 50
support in shock mcg/kg/minute, titrate to desired response;
infusion may be increased by 1-4 mcg/kg/minute
at 10- to 30-minute intervals until optimal
response is obtained
Note: If dosages >20-30 mcg/kg/minute are
needed, a more direct-acting vasopressor may be
more beneficial (i.e., epinephrine,
norepinephrine).
Hemodynamic effects of dopamine are dose
dependent:
 Low-dose: 1-5 mcg/kg/minute, increased renal
blood flow and urine output
 Intermediate-dose: 5-15 mcg/kg/minute,
increased renal blood flow, heart rate, cardiac
contractility, and cardiac output
 High-dose: >15 mcg/kg/minute, alpha-
adrenergic effects begin to predominate,
vasoconstriction, increased blood pressure
Enalaprilat Hypertensive 1.25 mg every six hours which might be increased
emergency to 5 mg every six hours
Enoxaparin Acute coronary 10 U (1 mg)/kg SC twice daily. An initial bolus 30
syndrome mg IV can be given.
Erythromycin Susceptible Oral: base: 250-500 mg every 6-12 hours
respiratory tract
infections
Erythromycin Susceptible Oral: base: 250-500 mg every 6-12 hours
respiratory tract
infections
Felodipine Hypertensive 5 mg orally
urgency
Furosemide Augmenting I.V.: 100-200 mg/dose, may be repeated or
diuresis in acute doubled in 1-2 hours as needed up to 1000 mg/day
renal failure Continuous I.V. infusion: Initial I.V. bolus dose of
 0.1 mg/kg followed by continuous I.V. infusion
doses of 0.1 mg/kg/hour doubled every 2 hours to
a maximum of 0.4 mg/kg/hour if urine output is <1
mL/kg/hour have been found to be effective and
result in a lower daily requirement of Furosemide
than with intermittent dosing.
Furosemide Hypertensive 20 mg orally if renal function is normal and higher
urgency if renal insufficiency is present
Gentamicin Septic shock Susceptible systemic infections: I.M., I.V.: Severe
life-threatening infections: 2-2.5 mg/kg/dose every
8 hours
Note: High-dose, once daily regimens: Some
clinicians suggest 4-7 mg/kg (as a single daily dose)
for all patients with normal renal function. This
dose is at least as efficacious with similar, if not
less, toxicity than conventional dosing.
Glyceryl trinitrate Acute coronary Sublingual: 0.5 mg every 5 min as needed x 3
syndrome doses.
IV: 10-200µg/min
Haloperidol Psychosis, 5-30mg/day
excitement,
aggression,
Agitation.
Hydralazine Hypertensive Initial dose: 10-20 mg/dose every 2-4 hours as
emergency needed. May increase to 40 mg/dose; change to
oral therapy as soon as possible
Hydrocortisone Acute asthma I.V. (succinate): 1-2 mg/kg/dose every 6 hours for
24 hours, then maintenance of 0.5-1 mg/kg every 6
hours
Hypertonic saline Hypotonic See section on “Hyperkalemia”
3% hyponatremia
Insulin Emergency Regular insulin, 5-10 units, plus dextrose 50%, 50
treatment of ml if plasma glucose is < 250 mg/dl
hyperkalemia
Ipratropium Acute asthma Nebulization: 500 mcg (one unit-dose vial) 3-4
bromide times/day with doses 6-8 hours apart
Metered dose inhaler: 2 inhalations 4 times/day,
up to 12 inhalations/24 hours
Isosorbide dinitrate Acute coronary Sublingual: 5mg as needed. Repeat every 5 min X
syndrome 3 doses.
Oral: 10 -20 mg BD or TDS
IV: Mix with D5w. 1-10 mg/hr
Isosorbide Prophylaxis of Regular tablet: 5-10 mg twice daily. Extended
mononitrate variceal bleeding release tablet: Initial: 30-60 mg given in morning
as a single dose; titrate upward as needed, giving
at least 3 days between increases; maximum daily
single dose: 240 mg
Labetalol Hypertensive Bolus: 20 mg initially, followed by 20 to 80 mg
 emergency every 10 minutes to a total dose of 300 mg.
Infusion: 0.5 to 2 mg/min
Labetalol Hypertensive Orally: 200-400 mg, may be repeated every 2-3
urgency hrs.
Labetalol Acute lowering of I.V. bolus: 20 mg I.V. over 2 minutes, may give 40-
blood pressure in 80 mg at 10-minute intervals, up to 300 mg total
acute stroke when dose.
indicated I.V. infusion: Initial: 2 mg/minute; titrate to
response up to 300 mg total dose. Administration
requires the use of an infusion pump.
Lactulose Hepatic Oral: 20-30 g (30-45 mL) every 1-2 hours to
encephalopathy induce rapid laxation; adjust dosage daily to
produce 2-3 soft stools; doses of 30-45 mL may be
given hourly to cause rapid laxation, then reduce
to recommended dose; usual daily dose: 60-100 g
(90-150 mL) daily
Lorazepam Status epilepticus I.V.: 4 mg/dose given slowly over 2-5 minutes;
may repeat in 10-15 minutes; usual maximum
dose: 8 mg
Lorazepam Hypnotic, 2-6mg/day
sedative,
anxiolytic.
Methylprednisolone Acute asthma I.V. (sodium succinate): Loading dose: 2
mg/kg/dose, then 0.5-1 mg/kg/dose every 6 hours
for up to 5 days
Methylprednisolone Acute asthma I.V. (sodium succinate): Loading dose: 2
mg/kg/dose, then 0.5-1 mg/kg/dose every 6 hours
for up to 5 days
Metolazone Augmenting Oral: 5-20 mg/dose every 24 hours.
diuresis in acute
renal failure
Metronidazole Amebiasis and Oral: 500-750 mg every 8 hours for 5-10 days
amebic liver
abscess
Midazolam Status epilepticus I.V. bolus: 0.2 mg/kg followed by continuous
infusion at rates of 0.75 to 10 µg/kg per minute
Neomycin Hepatic Oral: 500-2000 mg every 6-8 hours or 4-12 g/day
encephalopathy divided every 4-6 hours for 5-6 days
Nicardipine Hypertensive Initial dose: 5 mg/h; maximum dose: 15 mg/h IV
emergency infusion
Nimodipine Subarachnoid 60 mg every 4 hours for 21 days, start therapy
hemorrhage within 96 hours after the bleed.
Nitrofurantoin Urinary tract Oral: 50-100 mg/dose every 6 hours (not to exceed
infection 400 mg/24 hours)
Nitroglycerin Hypertensive 15 µg IV bolus, then 5-100 mcg/min (50 mg in 250
emergency mL D5W); maximum dose: 100 µg/min
Nitroprusside Hypertensive Initial dose: 0.25 to 0.5 µg/kg per min; maximum
sodium emergency dose: 8 to 10 µg/kg per min
Norepinephrine Hemodynamic Continuous I.V. infusion:
support in shock Adults: Initial: 0.5-1 mcg/minute and titrate to
desired response; 8-30 mcg/minute is usual range;
ACLS dosing range: 0.5-30 mcg/minute
Rate of infusion: 4 mg in 500 mL D5W
 2 mcg/minute = 15 mL/hour
 4 mcg/minute = 30 mL/hour
 6 mcg/minute = 45 mL/hour
 8 mcg/minute = 60 mL/hour
 10 mcg/minute = 75 mL/hour
Norfloxacin Urinary tract Oral: 400 mg twice daily for 3-21 days depending
infection on severity of infection or organism sensitivity;
maximum: 800 mg/day
Octreotide Upper GI I.V. bolus: 25-50 mcg followed by continuous I.V.
hemorrhage infusion of 25-50 mcg/hour
Pamidronate Hypercalcemia 60-90 mg, as a single dose, given as a slow infusion
over 2-24 hours; dose should be diluted in 1000
mL 0.45% NaCl, 0.9% NaCl, or D5W
Paracetamol Pain or fever Oral, 1000 mg 3-4 times /day; rectal: 325-650 mg
every 4-6 hours, do not exceed 4 g/day.
Phenobarbital Status epilepticus Loading dose: I.V.: 300-800 mg initially followed
by 120-240 mg/dose at 20-minute intervals until
seizures are controlled or a total dose of 1-2 g
Phenylephrine Hemodynamic I.M., S.C. : 2-5 mg/dose every 1-2 hours as needed
support in shock (initial dose should not exceed 5 mg)
I.V. bolus: 0.1-0.5 mg/dose every 10-15 minutes as
needed (initial dose should not exceed 0.5 mg)
I.V. infusion: 10 mg in 250 mL D5W or NS
(1:25,000 dilution) (40 mcg/mL); start at 100-180
mcg/minute (2-5 mL/minute; 50-90 drops/minute)
initially; when blood pressure is stabilized,
maintenance rate: 40-60 mcg/minute (20-30
drops/minute); rates up to 360 mcg/minute have
been reported; dosing range: 0.4-9.1
mcg/kg/minute
Phenytoin Status epilepticus I.V.: Loading dose: 20 mg/kg; maintenance dose:
300 mg/day or 5-6 mg/kg/day in 3 divided doses or
1-2 divided doses using extended release
Prednisolone Acute asthma Oral: 1-2 mg/kg/day in divided doses 1-2 times/day
for 3-5 days; most effective if ingested at about 3
pm
Procyclidine Drug-induced 7.5-30mg/day
extrapyramidal
symptoms.
Propofol Status epilepticus I.V.: 2 mg/kg over 10 minutes. If the seizures stop
prior to the infusion of the entire bolus, the bolus
should be discontinued and a continuous infusion
begun at 4 to 12 mg/kg per hour. This infusion
 should be titrated over the next 20 to 60 minutes
to maintain a seizure-free state and burst
suppression on the EEG.
Keep pressors at bedside and continuously
monitor BP and EEG.
Propranolol Acute coronary 10-80(usually 20-40 mg) mg orally 2-3 times daily.
syndrome For IV use give 0.5-1 mg IV followed 2 hrs later
with the oral dose.
Prophylaxis of 20mg every 12hrs, which is increased or decreased
variceal bleeding every 3-4 days until a 25% reduction in the resting
heart rate occurs or the heart rate is down to 55
beats per minute. Average dose is 40mg bid.
Reteplase Acute Coronary 10 units IV over 2 min then 30 min later another
Syndrome 10 units IV over 2 min (see section on Acute
Coronary Syndrome)
Rifampicin Meningococcal Oral: 600 mg every 12 hours for 2 days
meningitis <1 month: 10 mg/kg/day in divided doses every 12
prophylaxis hours for 2 days
Infants and Children: 20 mg/kg/day in divided
doses every 12 hours for 2 days
Salbutamol Emergency Nebulized salbutamol, 10-20 mg in 4 ml normal
treatment of saline, inhaled over 10 minutes
hyperkalemia
Salbutamol (via a Acute asthma Inhalation: 90 mcg/puff: 4-6 puffs every 20
nebulizer OR a minutes for up to 4 hours, then every 1-4 hours as
metered dose needed.
inhaler with a Nebulization: 2.5 mg diluted to a total of 3 mL by
spacer) continuous flow nebulization every 20 minutes for
three doses. May also give via continuous
nebulization, administering approximately 10 mg
over one hour.
Sodium bicarbonate Emergency 44-88 meq (1-2 ampoules) IV
treatment of
hyperkalemia
Streptokinase Acute Coronary 1.5 million units IV over 30-60 min (see section on
Syndrome Acute Coronary Syndrome)
Terlipressin Upper GI I.V.: Adults: 2 mg followed by 1 or 2 mg every 4
hemorrhage hours until bleeding is controlled, for up to 36
hours
Trimethoprim- Urinary tract Oral: 1 double strength tablet every 12 hours for
sulfamethoxazole infection, bacillary 10-14 days
dysentery
Unfractionated Acute coronary 60 U/kg IV bolus (max 5000 U) followed by 15
Heparin syndrome U/kg/hr (max 1000/hr). Adjust rate to aPTT 60-
80s.
Vasopressin Upper GI Continuous I.V. infusion: 0.5 milliunits/kg/hour
hemorrhage (0.0005 unit/kg/hour); double dosage as needed
every 30 minutes to a maximum of 10
 milliunits/kg/hour
I.V.: Initial: 0.2-0.4 unit/minute, then titrate dose
as needed; if bleeding stops, continue at same dose
for 12 hours, taper off over 24-48 hours.
Warfarin Acute embolic Start 5-10 mg daily for 2 days. Adjust dose
stroke due to according to INR results; usual maintenance dose
atrial fibrillations ranges from 2-10 mg daily
Zoledronic acid Severe or 4 mg (maximum) given as a single dose infused
symptomatic over no less than 15 minutes; patients should be
hypercalcemia adequately hydrated prior to treatment (restoring
urine output to ~2 L/day). Monitor serum calcium
and wait at least 7 days before considering
retreatment. Dosage adjustment may be needed in
patients with decreased renal function following
treatment.
Zuclopenthixol Psychosis, 50-150mg/day
excitement,
aggression,
Agitation.