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    Comatose PT

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    Nina
    This document provides an overview of managing a comatose patient. It discusses the anatomy and causes of coma, immediate assessment including Glasgow Coma Scale, differential diagnosis, important investigations, and general treatment approaches. The goal is to identify the underlying cause, stabilize the patient's condition by addressing issues like hypotension and hypoxia, and provide specific treatments when possible, such as for drug overdoses or basilar artery thrombosis. Care must be taken to avoid exacerbating issues like brain edema.

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    Comatose PT

    Uploaded by

    Nina
    43 views20 pages
    This document provides an overview of managing a comatose patient. It discusses the anatomy and causes of coma, immediate assessment including Glasgow Coma Scale, differential diagnosis, important investigations, and general treatment approaches. The goal is to identify the underlying cause, stabilize the patient's condition by addressing issues like hypotension and hypoxia, and provide specific treatments when possible, such as for drug overdoses or basilar artery thrombosis. Care must be taken to avoid exacerbating issues like brain edema.

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    comatose pt

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    This document provides an overview of managing a comatose patient. It discusses the anatomy and causes of coma, immediate assessment including Glasgow Coma Scale, differential diagnosis, important investigations, and general treatment approaches. The goal is to identify the underlying cause, stabilize the patient's condition by addressing issues like hypotension and hypoxia, and provide specific treatments when possible, such as for drug overdoses or basilar artery thrombosis. Care must be taken to avoid exacerbating issues like brain edema.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    43 views20 pages

    Comatose PT

    Uploaded by

    Nina
    This document provides an overview of managing a comatose patient. It discusses the anatomy and causes of coma, immediate assessment including Glasgow Coma Scale, differential diagnosis, important investigations, and general treatment approaches. The goal is to identify the underlying cause, stabilize the patient's condition by addressing issues like hypotension and hypoxia, and provide specific treatments when possible, such as for drug overdoses or basilar artery thrombosis. Care must be taken to avoid exacerbating issues like brain edema.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    of 20

    Management of a

    comatose patient
    By
    Yunus Ramadhan MBChB 5
    Facilitator: Dr Ssebuliba m
    Date 31/10/2019
     Introduction
     Anatomy and physiology of coma
     History
     Immediate assessment
     General examination
     Brain stem reflexes
     Differential diagnosis of coma
     Investigations
     Treatment of coma
    Introduction

     Is unarousable unresponsiveness/ unawareness for more than one hour


     Coma accounts for a substantial amount of admission on emergency wards
     It demands immediate attention and an organized approach
    Anatomy and physiology of coma

     Almost all instances of diminished alertness can be traced to wide spread


    abnormalities of the cerebral hemispheres or to reduced activity of the
    reticular activating system (RAS). The proper functioning of this system ， its
    ascending projeιtions to the cortex ， and the cortex itself are required to
    maintain alertness and coherence of thought. It follows that the principal
    causes of coma are
     lesions that damage the RAS in the upper midbrain or its projections;
     destruction of large portions of both cerebral hemispheres;
     suppression of reticulocerebral function by drugs ， toxins ， or metabolic
    derangements such as hypoglycemia, anoxia ， uremia ， and hepatic
    failure.
     The proximity of the RAS to midbrain structures that control pupillary
    function and eye movements permits clinical localization of the cause of
    coma in many cases. eg
     Pupillary enlargement with loss of light reaction and loss of vertical and
    adduction movements of the eyes suggests that the lesion is in the upper
    brainstem where the nuclei subserving these functions reside.
     Conversely ， preservation of pupillary light reactivity and of eye
    movements absolves the upper brainstem and indicates that widespread
    structural lesions or metabolic suppression of the cerebral hemispheres is
    responsible for coma.
    History

     The cause of coma may be immediately evident as in cases of trauma ，


    cardiac arrest, or observed drug ingestion. In the remainder, certain points
    are useful: eg
     the circumstances and rapidity with which neurologic symptoms developed;
     the antecedent symptoms (confusion, weakness, headache, fever ，
    seizures, dizziness, double vision, or vomiting);
     the use of medications, drugs, or alcohol; and
     chronic liver ， kidney ， lung ， heart ， or other medical disease
    Direct interrogation of family ， observers ， and ambulance technicians on the
    scene, in person or by telephone, is an important part of the evaluation when
    possible
    Immediate assessment

     For trauma patients complete exposure is necessary and ‘log roll’ to examine
    the back and adequate stabilization of the neck
     The Glasgo coma scale is important in determining the severity of the coma
    and the subsequent management

     A GCS of 8 and below is defined as coma


    General examination

     Pulse
     Blood pressure
     Temperature
     Respiratory rate
     Skin
     Odour of the breathe
    Posturing
    Brainstem reflexes are also examined

     Pupillary reflex
     Ocular movement
     Corneal reflex
     Respiratory pattern

    As a rule coma due to bilateral hemispheral disease preserves these brainstem


    activities
    Differential diagnosis

     Diseases that cause no focal or lateralizing neurologic signs ， usually with


    normal brainstem functions; CT scan and cellular content of the CSF are
    normal
     a. Intoxications: alcohol ， sedative drugs ， opiates ，
     b. Metabolic disturbances: anoxia ， hyponatremia ， hypernatremia ，
    hypercalcemia ， diabetic acidosis ， non ketotic hyperosmolar
    hyperglycemia, hypoglycemia ， uremia, hepatic coma, hypo- and
    hyperthyroid states ， profound nutritional deficiency
    c. Severe systemic infections: pneumonia ， septicemia ， typhoid fever ，
     Malaria, Waterhouse-Friderichsen syndrome
     d. Shock from any cause
    e. Post seizure states ， status epilepticus ， nonconvulsive status epilepticus
    f. Hypertensive encephalopathy ， eclampsia
    g. Severe hyperthermia ， hypothermia
    h . Concussion
    i. Acute hydrocephalus
    2. Diseases that cause meningeal irritation with or without fever, and with an
    excess of WBCs or RBCs in the CSF ， usually without focal or lateralizing
    cerebral or brainstem signs; CT or MRI shows no mass lesion
    a. Subarachnoid hemorrhage from ruptured aneurysm, arteriovenous
    malformation, trauma
    b. Acute bacterial meningitis
    c. Viral encephalitis
    d. Miscellaneous: fat embolism, cholesterol embolism, carcinomatous and
    Iymphomatous meningitis
     3. Diseases that cause focal brainstem or lateralizing cerebral signs ， with or
    without changes in the CSF; CT and MRI are abnormal
    a. hemisphere hemorrhage (basal ganglionic, thalamic) or infarction ( Large
    middle cerebral artery territory) with secondary brain stem compression
    b. brainstem infarction due to basilar artery thrombosis or embolism
    c. brain abscess ， subdural empyema
    d. Epidural and subdural hemorrhage ， brain contusion
    e. brain tumor with surrounding edema
    Investigations

     The studies that are most usefull in the diagnosis of coma are chemical
    toxicologic analysis of blood and urine ，
     cranial CT or MRI ， EEG ， and CSF examination. Arterial blood gas analysis
    is helpful in patients with lung disease and acid-base disorders. The metabolic
    aberrations commonly encountered in clinical practice are usually exposed by
    measurement of electrolytes ， glucose ， calcium ， osmolarity ， and
    renal (blood urea nitrogen) and hepatic (NH) function. Toxicologic analysis
    may be necessary in any case of acute coma where the diagnosis is not
    immediately clear.
    Treatment

     The immediate goal in a comatose patient is prevention of further nervous


    system damage. Hypotension ， hypoglycemia ， hypercalcemia ，
    hypoxia ， hypercapnia ， and hyperthermia should be corrected rapidly. An
    oropharyngeal airway is adequate to keep the pharynx open in a drowsy
    patient who is breathing normally. Tracheal intubation is indicated if there is
    apnea ， upper airway obstruction, hypoventilation ， or emesis ， or if the
    patient is liable to aspirate because of coma. Mechanical ventilation is
    required if there is hypoventilation or a need to induce hypocapnia in order to
    lower ICP.
     IV access is established ， and naloxone and dextrose are administered if
    narcotic overdose or hypoglycemia is a possibility; thiamine is given along
    with glucose to avoid provoking Wernicke's disease in malnourished patients.
     In cases of suspected basilar thrombosis with brainstem ischemia ， IV
    heparin or a thrombolytic agent is often used, after cerebral hemorrhage has
    been excluded by a neuroimaging study. Physostigmine may awaken patients
    with anticholinergic type drug overdose
     The use of benzodiazepine antagonists offers some prospect of improvement
    after overdose of soporific drugs and has transient benefit in hepatic
    encephalopathy. Certain other toxic and drug-induced comas have specific
    treatments such as fomepizole for ethylene glycol ingestion.
     Administration of hypotonic intravenous solutions should be monitored
    carefully in any serious acute brain ill ness because of the potential for
    exacerbating brain edema . Cervical spine
     injuries must not be overlooked ， particularly before attempting
    intubation or evaluation of oculocephalic responses. Fever and
     meningismus indicate an urgent need for examination of the CSF to diagnose
    meningitis. If the lumbar puncture in a case of suspected meningitis is
    delayed ， an antibiotic such as a third generation cephalosporin may be
    administered ， preferably after obtaining blood cultures.

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