NEUROLOGICAL EMERGENCY(COMA,SAH)

Dr .Shabbir2nd year PG

MD Emergency Medicine

COMA

• Coma is a state of reduced alertness and responsiveness from which the patient cannot be aroused.

• COMA is a common presenting complaint in the emergency department(ED).

• The presentation can be the manifestation of a wide spectrum of diseases, with the degree of impairment ranging along a continuum from sleepiness to decreased alertness to frank coma.

• Stupor-unresponsiveness from which patient can be arousal.

• Lethargy-decreased awareness and mental status

PATHOPHYSIOLOGY

• The pathophysiology of coma is complex.

• Coma can result from deficiency of substrates needed for neuronal function (metabolic).

• coma may result from a brainstem disorder such as haemorrhage or from bilateral cortical dysfunction.(structural)

causes

• Coma from causes affecting the brain diffusely METABOLIC.

• Coma from primary CNS disease or trauma STRUCTRAL.

METABOLIC

• Encephalopathies• Toxins• Drug reactions (e.g., neuroleptic malignant

syndrome)• Environmental causes—hypothermia,

hyperthermia• Deficiency state—Wernicke encephalopathy• Sepsis

• Hypoxic encephalopathy• Metabolic encephalopathy Hypoglycemia, Hyperosmolar state (e.g., hyperglycemia) Electrolyte abnormalities (e.g, hypernatremia , hyponatremia, hypercalcemia)

• Organ system failure• Hepatic encephalopathy• Uremia /renal failure• Endocrine (e.g., Addison disease, hypothyroidism, etc.)• Hypoxia• CO2 narcosis

• Hypertensive encephalopathy

STRUCTRAL

• Direct CNS trauma Diffuse axonal injury Subdural hematoma Epidural hematoma• 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 with both the depth of coma and the cause.

• Pupillary findings, cranial nerve evaluation, hemiparesis. These findings can assign the cause of the coma into a probable general category—diffuse CNS dysfunction (toxic-metabolic coma) or focal CNS dysfunction (structural coma).

Toxic-Metabolic Coma

• Patient demonstrates either spontaneous movements or reflex posturing, the movements are symmetric without evidence of hemiparesis.

• Muscle stretch reflexes, if present, are symmetric.

• Pupillary response is generally preserved in toxic-metabolic coma.

Coma from Supratentorial Lesions

• may present with progressive hemiparesis or asymmetric muscle tone and reflexes.

• Uncal herniation syndrome is an example of a supratentorial syndrome.

• medial temporal lobe shifts to compress the upper brainstem, which results in progressive drowsiness followed by unresponsiveness.

• The ipsilateral pupil is sluggish, eventually becoming dilated and nonreactive as the third cranial nerve is compressed by the medial temporal lobe.

• Hemiparesis may develop ipsilateral to the mass from compression of the descending motor tracts in the opposite cerebral peduncle.

Coma from Infratentorial Lesions

• cerebellar hemorrhage or infarction, may cause abrupt coma, abnormal extensor posturing, loss of pupillary reflexes, and loss of extraocular movements.

• pontine hemorrhage, which may present with the unique signs of pinpoint-sized pupils.

DIAGNOSIS

• Neurological evaluation• Lab investigations

Neurological evaluation

• Level of arousal• Posture• Brainstem reflexes• Pupil and eye examination• Neck rigidity

Level of arousal

• GLASGOW COMA SCALE• FOUR SCORE SCALE• AVPU SCALE

POSTURE

Brainstem reflexes

Lab investigations

• TO ROLE OUT METABOLIC CAUSE• TO ROLE OUT STRUCTRAL CAUSE

TO ROLE OUT METABOLIC CAUSE

• Complete blood count, MP• B.sugar• Blood urea, s. creatinine s.electrolyte• ABG, LFT- (S. AMMONIA)• THYROID FUNCTION TEST• CSF ANALYSIS• Toxicological studies

TO ROLE OUT STRUCTRAL CAUSE

• Noncontrast computed tomography (CT) of the brain is the initial imaging modality of choice in the setting of depressed consciousness and coma.

• Electrocardiograms (ECGs) can reveal cardiac ischemia, conduction blocks, or arrhythmia or can help corroborate certain ingestions (tricyclic antidepressants), electrolyte abnormalities (e.g.,potassium, calcium), or hypothermia.

TREATMENT

• IMMEDIATE MANAGEMENT• DEFNITVE MANAGEMENT

IMMEDIATE MANAGEMENT

• ABC of resuscitation.• IV access and oxygen therapy• Coma cocktail regimen• Cardiac monitor with pulse oxymetry• C spine stabilization

DEFNITVE MANAGEMENT

• Treat underlying cause.• Control of raised ICP.

SUBARACHNOID HAEMMORRHAGE

• The most common cause is trauma.

• Commonest cause for spontaneous SAH is saccular aneurysms.

• It compromises 6-8% of all strokes.

• Two percent of family members of patients with subarachnoid hemorrhage will develop the same disease.

• This risk rises with increasing number of family members involved or with a family history of adult polycystic kidney disease.

CLINICAL FEATURES

• Patients with subarachnoid haemorrhage classically present to the ED with the so-called thunderclap headache or a severe headache of acute onset that reaches maximal intensity within minutes.

• In the absence of blunt trauma, subhyaloid retinal haemorrhage is pathognomonic of subarachnoid haemorrhage but is seen in only 11% to 33% of cases.

• Patients may relate a history of a recent severe headache, generally thought to represent a “sentinel bleed.”

• Approximately 20% of patients develop their symptoms while engaged in activities that cause increased blood pressure, such as exercise, sexual intercourse, or defecation.

DIAGNOSIS

• The initial diagnostic modality of choice when subarachnoid haemorrhage is suspected is a noncontrast CT of the head.

• The sensitivity of modern CT in diagnosing subarachnoid hemorrhage is highest shortly after symptoms begin and is estimated to be 98% when performed within 12 hours of the onset of symptoms.

• most authorities agree that cerebrospinal fluid (CSF) analysis is required when a patient with suspected subarachnoid hemorrhage has a normal result on head CT scan.

• MRI is not as sensitive for detecting acute blood as CT scan.

• The two CSF tests of greatest interest in the evaluation of a patient for subarachnoid haemorrhage are the presence of xanthochromia and red blood cell (RBC) count

• Normal findings on head CT, the absence of xanthochromia, and zero or few RBCs (<5 × 106 RBCs/L) in the CSF reliably exclude subarachnoidhemorrhage.

• Unfortunately, the literature remains unclear on the threshold number of RBCs needed in the CSF to be considered diagnostic of subarachnoid hemorrhage.

• The addition of CT angiography to CT and LP shows promise for the ED diagnosis of aneurysmal subarachnoid hemorrhage.

TREATMENT

• The Glasgow Coma Scale (GCS) and pupillary responses should be checked regularly, because a decrease of one GCS point can indicate the onset of complications.• The risk of rebleeding is greatest in the first

24 hours and can be reduced by adequate blood pressure control.

• use of antifibrinolytics to prevent rebleeding after subarachnoid hemorrhage, but generally these are not used, because there is a risk of increased cerebral ischemia.

• Blood pressure may fluctuate through the course of the disease, a titratable IV antihypertensive, such as labetalol, is preferred.

• Vasospasm is most common 2 days to 3 weeks after subarachnoid hemorrhage.

• A modest protective benefit is seen with administration of nimodipine, 60 milligrams PO every 4 hours, and this therapy should be

initiated within 96 hours of symptom onset unless contraindicated due to allergy, non functioning GI tract, or hepatic disease.

• Surgery remains treatment of choice includes• Clipping of aneurysm,grade 2 and 3.• Endovascular coiling

DISPOSITION AND FOLLOW-UP

• All patients diagnosed with subarachnoid haemorrhage should be admitted to an intensive care unit in consultation with a neurosurgeon.

• patients who have normal findings on head CT and CSF analysis within 2 weeks of occurrence of initial symptoms may be safely discharged from the ED.