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Coma
M/I Ex
Disorders of consciousness may be divided into processes that affect either arousal functions, content of
consciousness functions, or combinations of both functions.
Arousal behaviors include wakefulness and basic eyes-open, alerting functions. Anatomically, neurons
responsible for these arousal functions reside in the reticular activating system, a collection of neurons scattered
through the midbrain, pons, and medulla.
Content of consciousness includes self-awareness, language, reasoning, spatial relationship integration,
emotions, and the myriad complex integration functions that we regard basic to being human. The neuronal
structures responsible for the content of consciousness reside in the cerebral cortex.
Dementia is failure of the content portions of consciousness with relatively preserved alerting functions.
Delirium is an arousal system dysfunction, and content of consciousness is affected as well.
Coma is failure of both arousal and content functions.
Coma is a state of reduced alertness and responsiveness from which the patient cannot be aroused.
Differential Diagnosis of Coma
Coma from Causes Affecting the Brain Diffusely
Encephalopathies
Hypoxic encephalopathy
Metabolic encephalopathy
Hypoglycemia
Hyperosmolar state (e.g., hyperglycemia)
Electrolyte abnormalities (e.g., hyper- or hyponatremia, hypercalcemia)
Organ system failure
Hepatic encephalopathy
Uremia/renal failure
Endocrine (e.g., Addison, hypothyroid, etc)
Hypoxia
CO2 narcosis
Hypertensive encephalopathy
Toxins
Drug reactions (e.g., neuroleptic malignant syndrome)
Environmental causes—hypothermia, hyperthermia
Deficiency state—Wernicke encephalopathy
Sepsis
Coma from Primary CNS Disease or Trauma
Direct CNS trauma
Vascular disease
Intraparenchymal hemorrhage (hemispheric, basal ganglia, brainstem, cerebellar)
Subarachnoid hemorrhage
Infarction
Hemispheric, brainstem
CNS infections
Neoplasms
Seizures
Nonconvulsive status epilepticus
Postictal state
Clinical Features
The clinical features of coma vary both with the depth of coma and the etiology.
A patient in coma with a hemispheric hemorrhage may still have some muscle tone; careful examination may
allow detection of decreased muscle tone on the side of the hemiparesis. The eyes may conjugately deviate
toward the side of the hemorrhage. With expansion of the hemorrhage and surrounding edema, increase in ICP,
or brainstem compression, unresponsiveness may progress to a complete loss of motor tone and loss of the
ocular findings as well.
Absence of localising CNS signs should point toward a more diffuse CNS dysfunction process such as toxicmetabolic coma.
Pseudocoma or psychogenic coma is occasionally encountered and may present a perplexing clinical problem.
Adequate history and observation of responses to stimulation will reveal findings that differ from the syndromes
described above. Pupillary responses, extraocular movements, muscle tone, and reflexes will be shown to be
intact on careful examination. Tests of particular value are observing the response of the patient to manual eyeopening (there should be little or no resistance in the truly unresponsive patient) and extraocular movements.
Specifically, if avoidance of gaze is consistently seen with the patient always looking away from the examiner,
or if nystagmus is demonstrated with caloric vestibular testing, this is strong evidence for nonphysiologic or
feigned unresponsiveness.
Diagnosis
In the approach to the comatose patient, stabilization, diagnosis, and treatment actions overlap and are often
performed simultaneously. Examination, laboratory procedures, and neuroimaging allow determination of the
cause of coma in almost all patients in the ED. As with any patient, airway, breathing, and circulation need to be
immediately addressed.
Reversible causes of coma, such as hypoglycemia or opiate overdose, should always be considered. Exploit all
possible historical sources (EMS personnel, caregivers, family, witnesses, medical records, etc.) to aid in
diagnosis.
History:
The tempo of onset of the coma is of great diagnostic value. Abrupt coma suggests abrupt CNS failure with
possible causes such as catastrophic stroke or seizures. A slowly progressive onset of coma may suggest a
progressive CNS lesion such as tumor or subdural hematoma. Metabolic causes such as hyperglycemia may also
develop over several days.
General examination:
May reveal signs of trauma or suggest other diagnostic possibilities for the unresponsiveness. For example, a
toxidrome may be present that suggests diagnosis and therapy, such as the hypoventilation and small pupils
found with opioid overdose. Signs of external trauma should be looked for including IV drug track marks.
Vitals:
 Pulse: tachycardia or bradycardia s/o toxidromes, raised intracranial pressures etc
 BP: as an aid in diagnosis and management of ICH, toxidromes, hypertensive encephalopathy e.g.
NMS. Hypotension characteristic of coma alcohol/barbiturate OD, internal hemorrhage, AMI, sepsis,
profound hypothyroidism or addisonian crisis.

Temparature: hypothermia in case of alcohol, barbiturate, sedative OD; hypoglycaemia and
hypothyroidism or hyperthermia in c/o anticholinergic toxidromes, heat stroke and sepsis
 Respiratory rate and patterns: apnea in opioid overdoses, tachypnea/ bradypnea in other toxidromes and
metabolic encephalopathy e.g. aspirin, uremia.
 Oxygen saturations: as an aid in diagnosis and management for hypoxic encephalopathy, respiratory
causes of sepsis
Bedside investigations:
 BSL: hypo- or hyperglycemia
 ECG: signs of toxidromes especially TCA overdose or prolonged QT interval
 Urine analysis: ketones, source of sepsis, content in uremia, specific tests as in toxidromes, drug
screening
 Arterial/venous blood gases: in c/o toxidromes and for management of significantly ill patient
Laboratory investigations:
 Blood investigations: electrolyte abnormalities, glucose, calcium levels, osmolarity and renal and
hepatic function tests(ammonia); ethanol levels (level of 43 mmol/L (0.2 g/dL) in nonhabituated
patients generally causes impaired mental activity and of >65 mmol/L (0.3 g/dL) is associated with
stupor. The development of tolerance may allow the chronic alcoholic to remain awake at levels >87
mmol/L (0.4 g/dL).
 Toxicology screen where appropriate: aspirin, valproate, carbamazepine etc.
Radiologic investigations:
 CXR: to rule out a primary sepsis cause or complications of coma e.g. aspiration pneumonia and in
case of trauma to rule out other injuries.
 CT brain: to rule out SOL, traumatic causes. Anatomic CNS lesions causing coma that cannot be
picked by CT include:o Bilateral hemisphere infarction,
o acute brainstem infarction,
o encephalitis, meningitis,
o mechanical shearing of axons as a result of closed head trauma,
o sagittal sinus thrombosis, and
o subdural hematomas that are isodense to adjacent brain
Other investigations of help in specific situations:
 EEG: useful in metabolic and drug induced states but rarely diagnostic, but helpful to diagnose
seizures, encephalitis due to HSV or prion disease.
o Predominant high-voltage slowing (δ or triphasic waves) in the frontal regions is typical of
metabolic coma, as from hepatic failure
o widespread fast (β) activity implicates sedative drugs (e.g., diazepines, barbiturates)
o A special pattern of "alpha coma," defined by widespread, variable 8- to 12-Hz activity,
superficially resembles the normal α rhythm of waking but is unresponsive to environmental
stimuli. It results from pontine or diffuse cortical damage and is associated with a poor
prognosis
 Lumbar puncture: examination of the CSF remains indispensable in the diagnosis of meningitis and
encephalitis.
 MRI
Treatment of Coma:
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.
Airway: An oropharyngeal airway is adequate to keep the pharynx open in drowsy patients who are 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.
Breathing: Mechanical ventilation is required if there is hypoventilation or a need to induce hypocapnia in order
to lower ICP.
Circulations: IV access is established, and
o naloxone and dextrose are administered if narcotic overdose or hypoglycemia are even remote
possibilities;
o thiamine is given along with glucose to avoid provoking Wernicke disease in malnourished patients.
o In cases of suspected basilar thrombosis with brainstem ischemia, IV heparin or a thrombolytic agent is
often utilized, after cerebral hemorrhage has been excluded by a neuroimaging study.
o Physostigmine may awaken patients with anticholinergic-type drug overdose but should be used only
by experienced physicians and with careful monitoring; many physicians believe that it should only be
used to treat anticholinergic overdose-associated cardiac arrhythmias.
o The use of benzodiazepine antagonists offers some prospect of improvement after overdoses of
soporific drugs and has transient benefit in hepatic encephalopathy.
o IV administration of hypotonic solutions should be monitored carefully in any serious acute brain
illness because of the potential for exacerbating brain swelling.
Cervical spine injuries must not be overlooked, particularly prior to attempting intubation or evaluating 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 for any reason, an antibiotic such as a thirdgeneration cephalosporin should be administered as soon as possible, preferably after obtaining blood cultures.
Prognosis
o Children and young adults may have ominous early clinical findings such as abnormal brainstem
reflexes and yet recover, so that temporization in offering a prognosis in this group of patients is wise.
o Metabolic comas have a far better prognosis than traumatic ones.
o All systems for estimating prognosis in adults should be taken as approximations, and medical
judgments must be tempered by factors such as age, underlying systemic disease, and general medical
condition.
o In an attempt to collect prognostic information from large numbers of patients with head injury, the
Glasgow Coma Scale was devised; empirically it has predictive value in cases of brain trauma. Patients
scoring 3 or 4 have an 85% chance of dying or remaining vegetative, while scores >11 indicate only a
5–10% likelihood of death or vegetative state and 85% chance of moderate disability or good recovery.
Intermediate scores correlate with proportional chances of recovery.
o For anoxic and metabolic coma, clinical signs such as the pupillary and motor responses after 1 day, 3
days, and 1 week have been shown to have predictive value.
o The absence of the cortical waves of the somatosensory evoked potentials has also proved a strong
indicator of poor outcome in coma from any cause.
Disposition
o Patients with readily reversible causes of coma, such as insulin-induced hypoglycemia, may be
discharged if home care and follow-up care are adequate and a clear cause for the episode is suspected.
o For patients with enduring altered consciousness, admission will be necessary. Most systems depend on
emergency physicians to stabilize the patient and correctly assign a tentative diagnosis so the patient
may be admitted to the proper specialty service.
o If the appropriate service is not available, transfer should be considered after stabilization.
Brain death
DIS H
This is a state of cessation of cerebral function while somatic function is maintained by artificial means and the
heart continues to pump. It is the only type of brain damage that is recognized as equivalent to death. Several
similar criteria have been advanced for the diagnosis of brain death, and it is essential to adhere to those
standards endorsed by the local medical community. Ideal criteria are simple, can be assessed at the bedside,
and allow no chance of diagnostic error.
They contain three essential elements of clinical evidence:
(1) widespread cortical destruction that is reflected by deep coma and unresponsiveness to all forms of
stimulation;
(2) global brainstem damage demonstrated by absent pupillary light reaction and by the loss of oculovestibular
and corneal reflexes; and
(3) destruction of the medulla manifested by complete apnea.
The pulse rate is invariant and unresponsive to atropine. Diabetes insipidus is often present but may develop
hours or days after the other clinical signs of brain death. The pupils are often enlarged but may be mid-sized;
they should not, however, be constricted. The absence of deep tendon reflexes is not required because the spinal
cord remains functional. There may or may not be Babinski signs.
Demonstration that apnea is due to irreversible medullary damage requires that the P CO2 be high enough to
stimulate respiration during a test of spontaneous breathing.
Apnea testing can be done safely by the use of diffusion oxygenation prior to removing the ventilator. This is
accomplished by preoxygenation with 100% oxygen, which is then sustained during the test by oxygen
administered through a tracheal cannula. CO2 tension increases ~0.3–0.4 kPa/min (2–3 mmHg/min) during
apnea. At the end of the period of observation, typically several minutes, arterial P CO2 should be at least >6.6–
8.0 kPa (50–60 mmHg) for the test to be valid. Apnea is confirmed if no respiratory effort is observed in the
presence of a sufficiently elevated PCO2.
The possibility of profound drug-induced or hypothermic depression of the nervous system should be excluded,
and some period of observation, usually 6–24 h, is desirable during which the signs of brain death are sustained.
It is advisable to delay clinical testing for at least 24 h if a cardiac arrest has caused brain death or if the inciting
disease is not known.
An isoelectric EEG may be used as a confirmatory test for total cerebral damage. Radionuclide brain scanning,
cerebral angiography, or transcranial Doppler measurements may also be used to demonstrate the absence of
cerebral blood flow but they have not been extensively correlated with pathologic changes.
Although it is largely accepted in western society that the respirator can be disconnected from a brain-dead
patient, problems frequently arise because of poor communication and inadequate preparation of the family by
the physician. Reasonable medical practice allows the removal of support or transfer out of an intensive care
unit of patients who are not brain dead but whose condition is nonetheless hopeless and are likely to live for
only a brief time.