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Neurology - Nihal > CN LANGE - Coma I > Flashcards

CN LANGE - Coma I Flashcards

1
Q

Coma results from …?

A

Disturbance in the function of EITHER the brainstem reticular activating system above the mid pons OR of BOTH cerebral hemispheres.

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2
Q

Emergency management of the comatose patient - Immediately:

A
  1. Ensure adequacy of airway, ventilation, and circulation. 2. Draw blood for serum glucose, electrolytes, liver and renal function tests, PT, PTT, and CBC. 3. Start IV and administer 25g of dextrose, 100mg of thiamine, and 0.4-1.2mg of naloxone IV. 4. Treat seizures.
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3
Q

Emergency management of the comatose patient - Next:

A
  1. If signs of meningeal irritation are present, perform LP to rule out meningitis. Obtain a history if possible. 2. Perform detailed general physical and neurologic examination. 3. Order CT scan of head if history or findings suggest structural lesion or SAH.
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4
Q

Emergency management of the comatose patient - Later:

A
  1. ECG. 2. Correct hyper/hypothermia. 3. Correct severe acid-base and electrolyte abnormalities. 4. CXR. 5. Blood and urine tox studies. 6. EEG.
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5
Q

Adequacy of ventilation can be established by …?

A
  1. The absence of cyanosis. 2. A respiratory rate greater than 8/min. 3. The presence of breath sounds on auscultation of the chest. 4. The results of arterial blood gas studies.
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6
Q

Flumazenil ( GABA antagonist to reverse sedation) 1 to 10mg IV, may be useful when benzodiazepine OD contributes to coma. However, …?

A

It should NOT be used in patients with: 1. History of seizures. 2. Chronic benzodiazepine use. 3. Suspected co-ingestion of tri- or tetracyclic antidepressants. ( anatgonises the effect of benzo - reducing seizure threhold)

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7
Q

Suspect ingestion of TCAs if?

A

The ECG shows: 1. Sinus tachycardia at a rate of 130/min or more. 2. QTc interval greater than 0.5sec. 3. QRS duration greater than 0.1sec.

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8
Q

History - The most crucial aspect of history is …?

A

The TIME OVER WHICH COMA DEVELOPS.

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9
Q

History - A sudden onset of coma suggests:

A

Vascular origin –> Especially a brainstem stroke or SAH.

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10
Q

History - Rapid progression from hemispheric signs, such as hemiparesis, hemisensory deficit, or aphasia, to coma within MINUTES to HOURS is characteristic of …?

A

INTRACEREBRAL HEMORRHAGE.

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11
Q

History - A more protracted course leading to coma (days to a week or more) is seen with:

A
  1. Tumor. 2. Abscess. 3. Chronic subdural hematoma.
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12
Q

History - Coma preceded by a confusional state or agitated delirium, without lateralizing signs or symptoms, is probably due to …?

A

A metabolic derangement or infection (meningitis, encephalitis).

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13
Q

Metabolic coma - DDx - Respiratory acidosis:

A
  1. Sedative drug intoxication. 2. Pulmonary encephalopathy - causes coma when arterial ph falls under 7.20 and paCO2 goes over 80mmHg)
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14
Q

Metabolic coma - DDx - Respiratory alkalosis:

A
  1. Hepatic encephalopathy. 2. Salicylate intoxication - result of ingestion of chemicals metabolised to salicylate e.g. asprin OD - nausea/vomiting/dizziness - hyperventilation -Resp Alkalosis - develop metabolic acidosis later on 3. Sepsis.
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15
Q

Metabolic coma - DDx - Metabolic acidosis:

A
  1. DKA. 2. Uremic encephalopathy - acquired toxic syndrome characterised by delirium in end stage renal disease 3. Lactic acidosis - build up of lactate due to nausea and vomiting 4. Methanol intoxication. 5. Ethylene glycol intoxication. 6. Isoniazid intoxication ( OD of antiobiotic drug for TB) 7. Salicylate intoxication. 8. Sepsis (terminal).
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16
Q

Metabolic coma - DDx - Metabolic alkalosis:

A

Coma unusual.

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17
Q

General physical examination - Signs of trauma - Inspection of the head may reveal signs of basilar skull fracture, including:

A
  1. Raccoon eyes - Periorbital ecchymoses. 2. Battle sign. 3. Hemotympanum. 4.CSF rhinorrhea or otorrhea.
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18
Q

Periorbital ecchymoses

A
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19
Q

battle sign

A
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20
Q

haemotympanum

A
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21
Q

CSF rhinorrhea

A

Cerebrospinal fluid (CSF) rhinorrhea is a condition where the protective fluid that surrounds the brain finds its way into the nose and sinuses, often appearing as a very watery runny nose. Most cases of CSF rhinorrhea occur after major accidents where the bones of the face and skull experience significant trauma

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22
Q

CSF rhinorrhea must be distinguished from other causes of rhinorrhea, such as allergic rhinitis:

A
  1. Glucose concentration does NOT reliably distinguish CSF from nasal mucus. 2. Beta-2 transferrin is UNIQUE to CSF, and its presence documents a CSF source of rhinorrhea.
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23
Q

Hypothermia occurs in coma caused by:

A
  1. Ethanol or sedative drug intoxication. 2. Hypoglycemia. 3. Wernicke encephalopathy. 4. Hepatic encephalopathy. 5. Myxedema.
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24
Q

Coma with hyperthermia is seen in:

A
  1. Heat stroke. 2. Status epilepticus. 3. Malignant hyperthermia related to inhalational anesthetics. 4. Anticholinergic drug intoxication. 5. Pontine hemorrhage. 6. Certain hypothalamic lesions.
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25
Q

General exam - Signs of meningeal irritation:

A
  1. Can be invaluable in the prompt diagnosis of meningitis or SAH. 2. BUT these signs are lost in deep coma, so their absence does NOT exclude these conditions.
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26
Q

General exam - Optic fundi - May reveal:

A

Papilledema or retinal hemorrhages compatible with chronic or acute HTN, or an elevation in intracranial pressure.

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27
Q

General exam - Optic fundi - What finding in an adult strongly suggest SAH?

A

Subhyaloid (superficial retinal) hemorrhages.

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28
Q

Neurologic exam:

A

The key to ETIOLOGIC DIAGNOSIS in the comatose patient.

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29
Q

Neurologic exam - What should be evaluated in detail?

A
  1. Pupillary size + reactivity. 2. Reflex eye movements (oculocephalic, oculovestibular reflexes). 3. Motor response to pain.
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30
Q

Pupils - Normal:

A

Typically 3-4mm in diameter (larger in children, smaller in elderly).

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31
Q

Normally reactive pupils in a comatose patient are characteristic of a …?

A

METABOLIC cause.

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32
Q

Thalamic pupils:

A

Slightly smaller (2mm) reactive pupils –> Early stages of thalamic compression from mass lesions, perhaps because of interruption of the DESCENDING SNS PATHWAYS.

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33
Q

Fixed, dilated pupils:

A

>7mm + fixed (unreactive to light) usually result from compression of the CN III (and associated SNS, pupillodilator fibers) anywhere along its course, from the midbrain to the orbit, but may also be seen in anticholinergic or SNS drug intoxication.

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34
Q

The MCC of a fixed dilated pupil in a comatose patient is …?

A

Transtentorial herniation of the medial temporal lobe from a supratentorial mass.

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35
Q

Fixed, midsized pupils:

A
  1. Pupils fixed at approx. 5mm in diameter are the result of brainstem damage at the MIDBRAIN level, which interrupts BOTH sympathetic pupillodilator, and parasympathetic, pupilloconstrictor nerve fibers.
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36
Q

Pinpoint pupils:

A

1-1.5mm in a comatose patient usually indicate opioid OD or, less commonly, a focal structural lesion in the pons.

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37
Q

Pinpoint pupils - How to distinguish opioid OD from focal structural lesion in the pons?

A
  1. Administration of naloxone. 2. Associated defects in horizontal eye movements that usually accompany pontine lesions.
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38
Q

Pinpoint pupils may appear unreactive to light except when …?

A

Viewed with a magnifying glass.

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39
Q

Pinpoint pupils can also be caused by …?

A
  1. Organophosphate poisoning. 2. Miotic eye drops. 3. Neurosyphilis (Argyll Robertson pupils).
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40
Q

Asymmetric pupils - Anisocoria:

A

Difference of 1mm or less in diameter is a normal finding that occurs in 20% of the population. –> Pupils constrict to a similar extent in response to light + extraocular movements are unimpaired.

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41
Q

Asymmetric pupils - A pupil that constricts less rapidly or to a lesser extent than its contralateral fellow usually implies …?

A

A structural lesion affecting the midbrain, oculomotor nerve, or eye.

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42
Q

Neurologic signs in coma with downward transtentorial herniation - In the early diencephalic phase:

A
  1. The pupils are small (approx. 2mm in diameter) + reactive. 2. Reflex eye movements are intact. 3. The motor response to pain is purposeful or semipurposeful (localizing) and often asymmetric.
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43
Q

Neurologic signs in coma with downward transtentorial herniation - In the late diencephalic phase:

A

Similar findings as in the early diencephalic phase, EXCEPT –> Painful stimulation results in decorticate (flexor) posturing, which may also be asymmetric.

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44
Q

Neurologic signs in coma with downward transtentorial herniation - With midbrain involvement:

A
  1. Pupils are fixed + midsized (approx. 5mm). 2. Reflex adduction of the eyes is impaired. 3. Pain elicits deCEREBRATE (extensor) posturing.
45
Q

Neurologic signs in coma with downward transtentorial herniation - Progression to involve the pons/medulla:

A
  1. Fixed, midsized pupils. 2. Loss of reflex abduction + adduction of the eyes. 3. NO motor response or only leg flexion upon painful stimulation.
46
Q

Note that although a lesion restricted to the pons produces pinpoint pupils as a result of the destruction of descending SNS (pupillodilator) pathways, downward herniation to the pontine level is associated with MIDSIZED pupils. This happens because herniation also interrupts …?

A

Parasympathetic (pupilloconstrictor) fibers in the oculomotor (III) nerve.

47
Q

Eye movements - Pathways tested:

A

The neuronal pathways examined by testing eye movements begin at the pontomedullary junction (VIII nerve and nucleus) –> Synapse in the caudal pons (horizontal gaze center and VI nucleus) –> Ascend through the central core of the brainstem reticular activating system (MLF) –> Arrive at the contralateral midbrain (III nerve and nucleus).

48
Q

Eye movements - Methods of testing:

A

In the comatose patient, eye movements are tested by: 1. Stimulating the vestibular system (semicircular canals of the middle ear) by passive head rotation (the oculocephalic reflex, or doll’s-head maneuver). 2. Using the stronger stimulus of ice-water irrigation against the tympanic membrane (oculovestibular reflex, or cold-water caloric testing).

49
Q

The doll’s-head (oculocephalic) maneuver is performed by:

A

Rotating the head horizontally to elicit horizontal eye movements + vertically to elicit vertical movements. –> The eyes should move in the direction opposite to that of head rotation.

50
Q

The oculocephalic maneuver may be …?

A

An INADEQUATE stimulus for inducing eye movements. –> The reflex may be overridden in conscious patients.

51
Q

Cold-water caloric (oculovestibular) stimulation:

A

More potent stimulus and is performed by irrigating the tympanic membrane with ice water.

52
Q

Cold-water caloric (oculovestibular) stimulation - In conscious patients:

A

Unilateral cold water irrigation produces NYSTAGMUS with the fast phase directed AWAY from the irrigated side.

53
Q

Cold-water caloric (oculovestibular) stimulation - In comatose patients with intact brainstem function:

A

Unilateral ice water irrigation results in TONIC DEVIATION of the eyes TOWARDS the irrigated side.

54
Q

An absent or impaired response to caloric stimulation with large volumes (eg 50mL) of ice water is indicative of …?

A
  1. Peripheral vestibular disease. 2. Structural lesion involving the posterior fossa (brainstem or cerebellum). 3. Intoxication with sedative drugs.
55
Q

Normal movements - A comatose patient with intact brainstem function has …?

A

Full conjugate horizontal eye movements, which occurs EITHER spontaneously (as “roving eye movements”) OR during the doll’s-head maneuver, as well as tonic conjugate deviation of BOTH eyes towards the side of the ice-water irrigation during cold-water caloric testing.

56
Q

Full horizontal eye movements in a comatose patient exclude:

A

A structural lesion in the brainstem as the cause of coma and suggest either a nonstructural (eg metabolic) cause or, less commonly, bilateral hemispheric lesions.

57
Q

Abnormal movements - Complete unresponsiveness to cold-water caloric testing in a comatose patient implies …?

A

Either a structural lesion of the brainstem affecting the pons OR a metabolic disorder that affects the brainstem preferentially, such as sedative drug intoxication.

58
Q

Abnormal movements - Downward deviation of one or both eyes in response to unilateral cold-water caloric testing also suggests …?

A

Sedative drug intoxication.

59
Q

The motor response to pain is assessed by applying strong pressure on the …?

A
  1. Supraorbital ridge. 2. Sternum. 3. Nail beds.
60
Q

Motor response to pain - The response to such stimuli can indicate whether the condition causing coma affects the brain …?

A

Symmetrically –> Typical of metabolic and diffuse disorders. Asymmetrically –> As in unilateral structural lesions.

61
Q

Motor response to pain - With cerebral dysfunction of only moderate severity, patients may …?

A

Localize an offending stimulus by reaching toward the site of stimulation. –> Although such “semipurposeful” localizing responses can be difficult to distinguish from the reflex responses, movements that involve LIMB ABDUCTION almost never represent reflex movements.

62
Q

Decorticate response to pain:

A
  1. Flexion of the arm at the elbow. 2. Adduction at the shoulder. 3. Extension + internal rotation of the leg + ankle.
63
Q

A decorticate response to pain is classically associated with lesions that involve the …?

A

Thalamus directly or large hemispheric masses that compress the thalamus from above.

64
Q

Decerebrate response to pain:

A
  1. Extension at the elbow. 2. Internal rotation at the shoulder + forearm. 3. Leg extension.
65
Q

Decerebrate response to pain tends to occur when brain dysfunction has descended to the level of …?

A

MIDBRAIN.

66
Q

Motor response to pain - Bilateral symmetric posturing may be seen in …?

A

BOTH structural + metabolic disorders.

67
Q

Motor response to pain - Unilateral or asymmetric posturing suggests …?

A

Structural disease in the contralateral cerebral hemisphere or brainstem.

68
Q

Motor response to pain - In patients with pontine and medullary lesions, there is usually …?

A

NO RESPONSE to pain, but occasionally some flexion at the knee (a spinal reflex) is noted.

69
Q

GCS - Eye opening:

A

1 –> None. 2 –> To pain. 3 –> To voice. 4 –> Spontaneous.

70
Q

GCS - Verbal response:

A

1 –> None. 2 –> Vocal but not verbal. 3 –> Verbal but not conversational. 4 –> Conversational but disoriented. 5 –> Oriented.

71
Q

GCS - Motor response:

A

1 –> None. 2 –> Extension. 3 –> Flexion. 4 –> Withdraws from pain. 5 –> Localizes pain. 6 –> Obeys commands.

72
Q

Pathophysiologic assessment - The most important step in evaluating a comatose patient is to …?

A

Decide whether the cause is a structural brain lesion (for which emergency neurosurgical intervention may be required) or a diffuse disorder caused by a metabolic disturbance, meningitis, or seizures (for which immediate medical treatment may be needed).

73
Q

Subtentorial structural lesions:

A
  1. Coma of sudden onset with focal signs of brainstem dysfunction strongly suggests a subtentorial structural lesion. 2. Abnormal pupillary function + impaired eye movement are the findings most suggestive of a subtentorial structural lesion, especially if asymmetric.
74
Q

Subtentorial structural lesions - Brainstem lesions may also be associated with:

A
  1. Conjugate gaze deviation away from the side of the lesion (and toward a hemiparesis). 2. Disconjugate eye movement such as INO.
75
Q

Are motor response helpful in separating supratentorial from subtentorial lesions?

A

NO.

76
Q

Ventilatory patterns associated with subtentorial lesions are …?

A

Abnormal but variable and may be ataxic or gasping.

77
Q

Ventilatory patterns in coma:

A
  1. Cheyne-Stokes respiration + central hyperventilation are seen with metabolic disturbances and with structural lesions at a variety of sites in the brain. 2. Ataxic + gasping ventilatory patterns are MC seen with pontomedullary lesions.
78
Q

Diffuse encephalopathies - Clinical presentation

A

Distinct from that of a mass lesion. 1. No focal signs (hemiparesis, hemisensory loss, or aphasia. 2. Consciousness is lost only gradually (except SAH), typically after a period of progressive somnolence or agitated delirium.

79
Q

Diffuse encephalopathies - A symmetric neurologic exam is the rule, although …?

A

Hypoglycemia, hyperosmolar nonketotic hyperglycemia, and hepatic encephalopathy may sometimes be accompanied by focal signs, such as hemiparesis, which may alternate from side to side.

80
Q

3 important clues that precede coma and suggest metabolic disease:

A
  1. Asterixis. 2. Myoclonus. 3. Tremor.
81
Q

Symmetric decorticate or decerebrate posturing can be seen with …?

A
  1. Hepatic. 2. Uremic. 3. Anoxic. 4. Hypoglycemic. 5. Sedative drug-induced coma.
82
Q

The hallmark of metabolic encephalopathy:

A

Reactive pupils in the presence of otherwise impaired brainstem function.

83
Q

A few metabolic causes of coma can also impair pupillary light reflexes, including:

A
  1. Massive barbiturate OD with apnea + hypotension. 2. Acute anoxia. 3. Marked hypothermia. 4. Anticholinergic poisoning (large pupils). 5. Opioid OD (pinpoint pupils). –> Even in these settings, completely unreactive pupils are uncommon.
84
Q

Pathophysiologic assessment of the comatose patient - Supratentorial structural lesion - Pupil size and light reaction:

A
  1. Usually normal size (3-4mm) and reactive. 2. Large (>7mm) and unreactive with transtentorial herniation.
85
Q

Pathophysiologic assessment of the comatose patient - Supratentorial structural lesion - Reflex eye movements:

A

Normal (gaze preference toward side of lesion may occur).

86
Q

Pathophysiologic assessment of the comatose patient - Supratentorial structural lesion - Motor responses:

A

Usually asymmetric - May be symmetric after transtentorial herniation.

87
Q

Pathophysiologic assessment of the comatose patient - Subtentorial structural lesion - Pupil size and light reaction:

A
  1. Midsized (about 5mm) + unreactive with midbrain lesion. 2. Pinpoint (1-1.5mm) + unreactive with pontine lesion.
88
Q

Pathophysiologic assessment of the comatose patient - Subtentorial structural lesion - Reflex eye movements:

A
  1. Impaired adduction with midbrain lesion. 2. Impaired adduction + abduction with pontine lesion.
89
Q

Pathophysiologic assessment of the comatose patient - Subtentorial structural lesion - Motor responses:

A

Asymmetric (unilateral lesion) or symmetric (bilateral lesion).

90
Q

Pathophysiologic assessment of the comatose patient - Diffuse encephalopathy/Meningitis - Pupil size and light reaction:

A
  1. Usually normal size (3-4mm) + reactive. 2. Pinpoint (1-1.5mm) + sometimes unreactive with opiates. 3. Large (>7mm) + unreactive with anticholinergics.
91
Q

Pathophysiologic assessment of the comatose patient - Diffuse encephalopathy/Meningitis - Reflex eye movements:

A

Usually normal. –> Impaired by sedative drugs or Wernicke encephalopathy.

92
Q

Pathophysiologic assessment of the comatose patient - Diffuse encephalopathy/Meningitis - Motor responses:

A
  1. Usually symmetric. 2. May rarely be asymmetric with hypoglycemia. 3. Hyperosmolar nonketotic hyperglycemia. 4. Hepatic encephalopathy.
93
Q

Subdural hematoma - In perhaps …% of cases a history of trauma is not present.

A

25%.

94
Q

Subdural hematoma - The classic history of waxing and waning signs and symptoms is …?

A

Too infrequent to be relied on for diagnosis.

95
Q

Subdural hematoma - Hemiparesis, when present, is contralateral to the lesion in approx. …% of cases.

A

70%.

96
Q

Subdural hematoma - Pupillary dilation, when present, is ipsilateral in approx. …% of cases.

A

90%.

97
Q

Clinical features of subdural hematoma - Acute - Symptoms:

A

100% –> Depressed consciousness. 24% –> Vomiting. 20% –> Weakness. 12% –> Confusion. 11% –> Headache. 6% –> Speech disturbances. 6% –> Seizures. 0% –> Vertigo + Visual disturbances.

98
Q

Clinical features of subdural hematoma - Acute - Signs:

A

100% –> Depressed consciousness. 57% –> Pupillary inequality. 44% –> Motor asymmetry. 17% –> Confusion + memory loss. 6% –> Aphasia. 1% –> Papilledema. 0% –> Hemianopia + facial weakness.

99
Q

Clinical features of subdural hematoma - Subacute - Symptoms:

A

88% –> Depressed consciousness. 44% –> Headache. 41% –> Confusion. 31% –> Vomiting. 19% –> Weakness. 8% –> Speech disturbance. 4% –> Vertigo. 3% –> Seizures. 0% –> Visual disturbance.

100
Q

Clinical features of subdural hematoma - Subacute - Signs:

A

88% –> Depressed consciousness. 37% –> Motor asymmetry. 27% –> Pupillary inequality. 21% –> Confusion and memory loss. 15% –> Papilledema. 12% –> Aphasia. 4% –> Hemianopia. 3% –> Facial weakness.

101
Q

Clinical features of subdural hematoma - Chronic - Symptoms:

A

81% –> Headache. 47% –> Depressed consciousness. 37% –> Confusion. 30% –> Vomiting. 22% –> Weakness. 12% –> Visual disturbance. 9% –> Seizures. 6% –> Speech disturbance. 5% –> Vertigo.

102
Q

Clinical features of subdural hematoma - Chronic - Signs:

A

59% –> Depressed consciousness. 41% –> Motor asymmetry. 27% –> Confusion and memory loss. 22% –> Papilledema. 20% –> Pupillary inequality. 11% –> Aphasia. 3% –> Hemianopia. 3% –> Facial weakness.

103
Q

Subdural hematoma - Acute/subacute/chronic?

A

Acute –> Within 3 days of trauma. Subacute –> 4-20 days. Chronic –> >20 days.

104
Q

Cerebral contusion:

A

Bruising of the brain caused by head trauma.

105
Q

Cerebral contusion - May be associated with:

A

Initial unconsciousness from which the patient recovers. –> Edema surrounding the contusion may cause the level of consciousness to fluctuate, and seizures + focal neurologic signs may develop.

106
Q

Cerebral contusion - Patients must be carefully monitored for …?

A

Neurologic deterioration related to progressive edema + herniation.

107
Q

Cerebral contusion - LP:

A

UNNECESSARY + potentially dangerous. –> CT/MRI are the diagnostic procedures of choice.

108
Q

In contrast to subdural/epidural hematomas, cerebral contusions …?

A

Rarely require surgery.

109
Q

Coma - Definition:

A

A sleep-like state with no purposeful response to the environment and from which the patient cannot be aroused. –> Unarousable unresponsiveness.

Neurology - Nihal (31 decks)

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