Occasion Title Objective Days/Date Presentant Supervisor Moderator Opponent

: Case Presentation : Subarachnoid Hemorrhage : To Discuss about diagnosis and Management : Saturday/August 25th 2011 : dr. Lydia Susanti : Prof. Dr. Basjiruddin Ahmad Sp.S(K) : Dr. Yuliarni Syafrita, SpS(K) : dr. Desi Suryani dan Dr. Dherma Putra

Spontaneus (nontraumatic) sub arachnoid hemorrhage (bleeding into the subarachnoid space) is usually the result of a ruptured cerebral arterial aneurysm or an AVMs. Intracranial AVMs, a less frequent cause of subarachnoid hemorrhage (10%), occur twice often in men and usually bleed in the second to fourth decades, although a significant incident extend into the sixties. 1

CASE ILUSTRATION A 49-year old male patient admitted to the neurology departement of Dr. M. Djamil hospital Padang on June 20th 2011

MAIN COMPLAINT Patient does not comprehend the contents of conversation and experience severe headache

HISTORY OF ILLNESS Suddenly patient could not comprehend the contents of conversation since 2 days before hospitalization. Patient mentioned that previous day he got a severe headache particularly on the back of head that he never felt before. In the morning the family looked the patient fell down and unconscious in the bathroom where vomit and feses around him. After a few minute the patient get general seizure, rigid for a few seconds, followed by the next seizures within 60 seconds. After that the patient remained unconscious. Then the patient was taken to Muaro Bungo Hospital. At the hospital, patient was awake but could not understand the contents of the conversation The next day the patient was referred to M. Djamil hospital Padang

HISTORY OF PAST MEDICAL ILLNESS He has a history of hypertension for 3 years, however he doesnot seek for a regularly treatment, some time he puts on medicine such as captopril and amlodipin. History of diabetes mellitus, heart disease or stroke was denied No history of head trauma.

HISTORY OF FAMILY ILLNESS Father and sibling of patients suffer from hypertension. No Family members suffer diabetes, heart disease and stroke. She has a wife and 3 children

SOCIAL BACKGROUND Patient was a civil servant, not drinking coffe,but smoking 12 cigarettes daily

PHYSICAL EXAMINATION General State Awareness Blood Pressure : Look sick : Alert : 160/100 mmHg Breathing Freq Temperature : 20 x/minute : 36,9 oC : 88 x/minute

Heart rate/Pulse freq

Internus State Eyes Neck Lungs Cor Abdomen : No anemic performance of conjuctiva or icteric sclera : JVP 5-2 cmH2O, left and rigt carotid bruit (-). : Within normal limits : Within normal limits : No bulge, liver and spleen not palpable.

Neurological State Alert, Glasgow pittsburg coma scale 12 Meningeal sign found : Nuchael rigidity but no signs of Brudzinski I, Kernig , Brudzinsky II No Sign of Increased of intracranial pressure Cranial Nerve : NI : Difficult assesed (aphasia)

 N II

: Isocor pupil, 2mm/2mm, reflex+/+

direct light reflex +/+,

indirect light

Funduscopi ODS : papil defined, orange, cupping (+) aa : vv 1 : 3, av.crossing (-). Hiperpigmentation (+), Sub hyaloids bleeding (-) : hypertension fundus KW I N III,IV,VI NV N VII N VIII N IX NX N XI N XII : dolls eyes movement (+) : Corneal reflex +/+ : facial simetry, lagoftalmus (-), right nasolabial fold flatter then the left nasolabial fold : occuloauditorik reflex +/+ : vomiting reflex (+) : Symmetrical pharyngeal, uvula is in the middle : difficult assesed : Deviation of tongue (-),atrophy (-), fasciculation (-)

Motoric : eutonus, eutrophy Muscle stregth : During the fall test look the left limb faster down. Sensoric : Respond to mild pain Otonom : Bladder attached catheter, no abnormality of prepiration Physiological Reflex : Reflex Biceps Triceps KPR APR Right ++ ++ ++ ++ Left ++ ++ ++ ++

Patologic reflex : Hoffman tromner (-/-), Babinski -/+, Oppenheim -/-, Chaddoks -/-, Schaefer -/-, Gordon -/-

Laboratory finding Hb WBCs Ht Platelets : 14 g/dL : 17.700 /mm3 : 43,2 % : 188.000 /mm
3

RBG Ureum Creatinin

: 119 mg/dL : 55 mg/dL : 1,4 mg/dL

Sodium

: 143 mmol/L

Potassiun : 3,9 mmol/L Chlorida : 108 mmol/L

ECG

: Sinus rhythm, HR 100 / min, ST depression (-), T inverted (-) SV1 + RV5<35 mm

Conclusion: Within normal limits Gajah Mada Algoritm : Unconciousness(+) Headache (-) Babinsky reflex (-) Conclusion : Haemorrhagic stroke

DIAGNOSIS Working Diagnosis Topical Diagnosis Etiology Diagnosis Secondary Diagnosis : Hemiparese dekstra + Sensoric Aphasia : Sub Arachnoid Space : Sub arachnoid Bleeding : Hypertension stage II

The results of brain CT scan without contrast : hyperdens lesion seen on the intersulci of left hemisphere. No midline shift. Ventricular system showed dilated, Pons and CVA is normal. Conclusion: sub-arachnoid haemorrhage

DIAGNOSIS Working Diagnosis Topical Diagnosis Etiology Diagnosis Secondary Diagnosis : Sub arachnoid hemorrhage stage II : Sub Arachnoid Space : Aneurisma Berry rupture : Hypertension stage II

MANAGEMENT: Head Elevation 30o 4

 IVFD RL 8 hours/kolf Diet ML RG II Folley catheter, monitor fluid balance Strick monitoring of seizure, fluid balance, natrium, stress ulcer He puts on medication : 1. Kalnex 6x1 gram (IV) 2. Nimotop infusion 2 cc/hour 3. Citicholin 2x500 mg (IV) 4. Dilantin 3 x 100 mg (Po) 5. Laxadin syrup 3x CI (Po)

NEXT INVESTIGATION : 1. Complete blood count: Hb, leukocytes, Diiferential counts, hematocrit, platelets, ESR, FBG and 2HPPG, total cholesterol, HDL, LDL, triglycerides, ureum, creatinine, uric acid, electrolytes (Na, K, Cl),Check the hemostatic physiology (PT, APTT) 2. Lumbar puncture 3. MRA (Magnetic Resonance Angiography) FOLLOW UP : 4th day Subjective (S): Speech disturbance, do not Understand the content of conversation, febrile (-), Bowel (-) 3 days Objective (O): Awareness, CM aphasia, BP 180/100 mmHg, pulse 80 / min, breathing 20x /min, T: 36.7 0C Alert, Glasgow pittsburg coma scale 12 Nuchal rigidity (+) Pupil isokor, 3mm/3mm, direct and indirect light reflex maneuvers (+/+), dolls eyes movement (+), right nasolabial fold is flatter Muscle strength : With the fall test, the right limb first falls Sensory: Response to mild pain (+) Autonomous: Bladder attached catheter, sweat secretion was normal Physiological reflex : Reflex Biseps Right ++ Left ++ 5

 Triseps KPR APR Patological reflex: -/-

++ ++ ++

++ ++ ++

MANAGEMENT: Head Elevation 30o IVFD RL 8 hours/kolf Diet ML RG II Folley catheter, monitor fluid balance Strick monitoring of seizure, fluid balance, natrium, stress ulcer He puts on medication : 1. Kalnex 6x1 gram (IV) 2. Nimotop infusion 2 cc/hour 3. Citicholin 2x500 mg (IV) 4. Dilantin 3 x 100 mg (Po) 5. Laxadin syrup 3x CI (Po) 5th day Subjective (S): Do not understand the content of conversation, febrile (-), Bowel (+). Patient experienced seizure for 1 minute, general seizure. Objective (O): Awareness CM aphasia, BP 160/100 mmHg, pulse 82 / min, breathing 21x / min, T: 36.7 0C Alert, Glasgow pittsburg coma scale 12 Nuchal rigidity (+) N. Cranial: Pupil isocor, 3mm/3mm direct and indirect light reflex maneuvers (+/+), dolls eyes move, right nasolabial fold flatter then the left one Muscle streght: With the fall test, the right limb falls first Sensoric: The response to mild pain (+) Autonomous: Bladder attached catheter, sweat secretion was normal

Physiological reflex : Reflex Biceps Triceps KPR APR Pathologic reflex: -/Right ++ ++ ++ ++ Left ++ ++ ++ ++

Laboratory : Hb 13,7 g/dL Leucocyte 13.900/mm3 Hematokrit 42% Platelet 190.000/mm3 Ureum 43 mg/dl Tot Colest 201 mg/dl HDL 47 mg/dl LDL 127 mg/dl Triglyseride 133 mg/dl PT 11,9 detik Creatinine 1,0 mg/dl Na 143 K 3,5 Cl 91 APTT 39,7 detik FBG 93 mg/dL Diff count 0/0/2/78/15/5 ESR 25 mm/hours

Brain CT Scan Results Ekspertise: Hyperdens lesion seen on parietal sulci and left-right frontotemporal area, particularly at the left side, as well as in sisterna and in the midline. Differentiation of the cortex and medulla are good (obviously). In some areas there is a narrowing in the anterior horn of lateral ventricle in infratentorial region. No midlineshift. Cerebellum, pons and CPA reveal within normal limit. Conclusion: Subrachnoid hemorrhage with cerebral edema in the infratentorial region. A : SubArachnoid Hemorrhage stage II

MANAGEMENT: Head Elevation 30o IVFD RL 8 hours/kolf Diet ML RG II Folley catheter, monitor fluid balance 7

 Strick monitoring of seizure, fluid balance, natrium, stress ulcer He puts on medication : 1. Kalnex 6x1 gram (IV) 2. Nimotop 4x60 mg (Po) 3. Citicholin 2x500 mg (IV) 4. Dilantin 3 x 100 mg (Po) 5. Laxadin syrup 3x CI (Po)

P:

Blood gas analysis

BGA Result: pH : 7,44 pH CO2 : 39 pO2 : 98 HCO3 : 26,4 SO2 : 98% Conclusion : Within normal limit The 6th day Subjective (S): Objective (O): Do not Understand the content of conversation, febrile (-), Bowel (+) Awareness CM aphasia, BP 140/80 mmHg, pulse 84 / min, breathing 22x / min, T: 36.9 0C Alert, Glasgow pittsburg coma scale 12 Nuchal rigidity (+) N. Cranial: Pupil isocor, 3mm/3mm, direct and indirect light reflex (+/+), dolls eyes move, right nasolabial fold flatter then flatter then the left one Muscle streght: With the fall test, the right limb falls first Sensoric: response to mild pain (+) Autonomous: Bladder attached catheter, sweat secretion was normal

Laboratorium : Cl :106 mmol/L K : 3,5 mmol/L Na : 140 mmol/L

Therapy Continued 10th day Laboratory Cl K Natrium Ureum Creatinine : 105 mmol/L : 3,6 mmol/L : 142 mmol/L : 32 mg/dl : 0,8 mg/dl

Ro Thoracic PA Expertise : Bronchovesikuler complexion within normal limits, CTR > 65% Conclusion : Cardiomegaly

Onset Day 23

MRA Result:

MRA Expertise : Dilatation of the left internal carotid artery and its branches with drainage into the venous sinus sigmoideus, sinus rectus. Conclusion AVM of the left carotid artery-sigmoid sinus rectus (the left)

Neurosurgery consultation: Estimate that there has been blockage/occlusion Feeding artery. Oclison feeding artery should be conducted in Jakarta.

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DISSCUSSION

A 49 year-old male patient who where admitted in neurology department. The diagnosis of sub-arachnoid hemorrhage . The diagnosis ha been established from the history of illness, physical examination and investigations. As the anamnesis it was found that patients suffered from severe headache which he never felt before suddenly a few hours before the patient lost of consciousness. Patient also experienced vomiting and convulsions shortly before being taken to Muaro Bungo hospital. From a physical examination at the time of entry was found that blood pressure of 160/100 mmHg. Meningeal signs: found nuchal rigidity, patients also experience sensory aphasia and right limb weakness. and from investigations Brain CT scan in ER support the diagnosis (Class I, Level of Evidence B) that is found in intersulci hiperdens lesions in the left hemisphere that are suitable with subarachnoid haemorrhage. Lumbar puncture (Class I, Level of Evidence B) have also been performed on these patients, but failed because of patient anxiety, after a second informed consent, the patient family refused to do a lumbar puncture. 2 The clinical presentation of SAH is usually quite distinctive. The classic description of a patient with SAH is one who describe his or her headache as the worst headache of my life. This often manifest as a sudden, severe, and unremitting headache, accompanied by nausea and vomiting. Photophobia, neck stiffness, and back pain can occur as a result of meningeal irritation. Meningismus my present consisting of nuchal rigidity or positive Brudzinsky or kernig sign. Impairment of concicousness may occur, as well as focal neurologic deficit.2,3 Non traumatic sub arachnoid hemorrhage (SAH) is an important cause of morbidity and mortality, caused by rupture of cerebral aneurism in most cases (80%). Cerebral

arteriovenous malformation (AVMs) are congenital vascular lesion that can present with SAH. There is no differences management between SAH caused by aneurism and SAH caused by AVMs. The differences are the treatment of causal. Although based on MRA that has been done for the patient was found AVMs, Aneurism as a risk factor for causal of sub arachnoid bleeding cannot be excluded. Because the patient has hypertension as a risk factor for aneurism. AVMs frequenly (10-20% incidence) accompanied by intracranial aneurism in feeding erteries, and these aneurism can be quite proximal and result in typical basal sub arachnoid hemorrhage like any other ruptured aneurysm 2,3,4 The degree of neurological imparment using an accepted SAH grading system can be useful for prognosis and triage (Class IIa, Level Evidence B). The modified Hunt and Hess 11

Grading scales serves as a means of risk stratification for SAH based on the first neurologic examination. General management of patients with head elevation 300, the infusion of NaCl 0.9% 8 hours / kolf, giving soft diet low salt II. While the specific therapy is Tranexamat Acid 1 gr/4 hour (IV), Nimodipin 2cc/hour infusion (day 3-7 maintainability), metabolic activator (Brain Act 250 mg/12 hour), and the provision of Phenytoin 100 mg/8 hour for 3 months, because the patients had seizures shortly before being taken to hospital. Folic Acid administration and 2 mg/24 hour .2,5 Although older studies demonstrated an overall negative effect of antifibrinolitics, recent evidence suggest that early treatment with a short course of antifibrinolitic agent, when combine with a program of early aneurism treatment followed by discontinuation of the antifibrinolitic and profilaxis agains hipovolemia and vasospasme may be reasonable, but further research is needed.2 Blood pressure should be monitored and controlled to balance the risk of stroke, hypertension related rebleeding, and maintenance the cerebral perfusion pressure. Neurologic complication are common and include symptomatic vasospasme (46%), hydrochefalus (29%), and rebleeding (7%). Some such as hyponatremia, seizure, neurogenic pulmonary edema, or cardiogenic dysfunction.2,3,6 Delayed cerebral ischemic from vasospasme accounts fo a large proportion of morbidity and mortality after SAH. Progresive arterial narrowing develop after SAH approximately 70% patient, but delayed ischemic deficit develop only 20-30%. The process begins 3-5 days after hemorrhage, becomes maximal at 5-14 days, and gradually resolves over 2-4 weeks. Simptomatic vasospasm usually involves a decrease in the level conscicousness, hemiparese or both. This patient suspected of having vasospasm, which was found lateralization to the right, and the patients had sensory aphasia. On MRI investigations conducted at the onset of day 21, were also found signs of infarction in the left temporo parietal.2,6,7

Magnetic Resonance Imaging

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Treatment of cerebral vasospasm begins with early management of ruptured aneurism, an in most cases maintaining normal circulation blood volume and avoiding hypovolemia is probably indicated. One reasonable approach to symptomatic cerebral vasospasm is volume expansion, induction of hypertension, and hemodilution (Triple H therapy). Oral nimodipin is indicated to reduce outcome related to aneurismal sub arachnoid hemorrhage.2,6,7 Clinically obvious tonic-clonic seizure occur in 5% SAH Patient during hospitalization and in another in the first years after discharge. Seizure after SAH are related primarily to focal pathology, including large sub arachnoid cloth, subdural hematom and cerebral infarction. Administration of anticonvulsant in emergency room to minimize the risk of acute seizure activity (IV phenitoin 20 mg/kg) is commonly used but routinely administered anticonvulsant after SAH are not well establish. Patients experiencing tonicclonic seizures at onset, and on day 3 of onset. In patients given phenytoin 3 x 100 mg orally.2,3,7 After a Magnetic Resonance Imaging and Magnetic Resonance Angiography considerable Arteriovena malformation in the left internal carotid artery - the sigmoid sinus and the sinus rectus. It also found some other AVM in the brain parenchyma. AVM is a congenital abnormality that occurs where there is a direct connection between arteries and veins without the discovery of capillaries. Most of the AVM (90%) were in supratentorial and in the parietal cortex. But basically the AVM can occur in all areas of the brain and the spinal cord. AVM in the posterior fossa has a morbidity and mortality is higher when compared with untreated control in the supratentorial AVM. Small AVM nidus with a diameter of 3 cm have a greater bleeding risk than large-sized AVM (neurosurgery) 8,9,10

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CONCLUSION

1. Subarachnoid hemorrhage that occurred in these patients was thought to be caused by rupture of arteriovenous malformations, eventhough SAH caused by aneurism can not be excluded. 2. Both management of SAH caused by aneurism or arteriovenous malformation are the same. The difference lies in the management of the etiology of SAH. 3. Patient is encouraged to perform occlusion of feeding arteries to Jakarta, but the family still reconsider. 4. Once the acute phase has passed and the conditions improved, the patient was discharged with the recommendation not to do heavy physical activity and straining. 5. Patient is suggested for routine control and monitor

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DAFTAR PUSTAKA

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Roger P. Simon, David A Greenberg, Michael J. Aminof. Clinical Neurology. 3 edition, New York, 2009.7;75-76

2.

Brisman JL, Mayberg MR. Subarachnoid Hemorrhage. In : Goldstein LB, ed. A Primer on Stroke Prevention Treatment and Treatment. Dallas, 2009.6;65-84

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Guideline Stroke 2007, Kelompok studi stroke PERDOSSI Kaibara T, Heroes CR, Arteriovenous Malformations of the Brain. In: Capplan LR Uncommon Cause of stroke. Cambridge University Press, 2 ed, New York, 2008;181187

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Miller M and Sinson G. Sub arachnoid hemorrhage. In: Torbey MT. Neurocritical care. Cambridge University Press, first edition, Cambridge, 2010; 167-185

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Suarez JI, Tarr RW, Selman WR. Current Concepts Aneurysmal Subarachnoid Hemorrhage. The New England Journal of Medicine. January 2006.

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Meyer SA, Bernardini GL. Sub arachnoid Hemorrhage. In:Rowland LP, Timothy A. Merrits Neurology. Lippincott Williams & Wilkins, 12 ed.New York.2010

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Gilroy J. Intracerebral, Subaracnoid, Pontine, and Intracerebelar Hemorrhage. Basic Neurology 3rd Ed, 2000. 10; 297-306

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Wismaji Sadewo. Arterivena Malformasi. Dalam Sinopsis Bedah Saraf. Departemen Bedah Saraf FKUI. Sagung Seto. Jakarta.2011

10. Tugasworo D. Perdarahan subarachnoid. Dalam:Syahrir H, Anwar Y, Kadri AS (editor); Neurology Update 2009. Perdosi Medan : 178-184.

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