- 1 1. Define coma. How is it different from stupor or obtundation?
- 2 2. What parts of the brain must be affected to produce coma?
- 3 3. How does coma change emergency management?
- 4 4. Describe the initial treatment of comatose patients.
- 5 5. How does a history of trauma affect emergency management of coma?
- 6 6. When should mannitol be used in patients with increased intracranial pressure? What are the contraindications?
- 7 7. What are the general pathophysiologic categories of coma?
- 8 8. Describe the diagnostic approach to comatose patients.
- 9 9. What initial laboratory evaluations should be performed in comatose patients?
- 10 10. What are the major causes of coma?
- 11 11. Describe changes in pupil size, position, and reaction to light that help to determine location and severity of disease.
- 12 12. What abnormal breathing patterns may be seen in comatose patients?
- 13 13. What is the oculovestibular reflex? How can it be used to assess comatose patients?
- 14 14. What is hepatic encephalopathy?
- 15 15. How is hepatic encephalopathy diagnosed?
- 16 16. What treatments are available for patients with hepatic encephalopathy?
1. Define coma. How is it different from stupor or obtundation?
Coma is a disorder of consciousness defined by absence of awareness. The comatose animal appears asleep but is unable to respond to external stimuli or physiologic needs except by reflex activity. Stupor implies a state of depressed consciousness responsive to some stimuli, even though it may lapse back into unconsciousness when the stimulus is withdrawn. An animal is considered obtunded when it is not alert, when it is disinterested in its environment, or when it has a less than normal response to external stimuli.
2. What parts of the brain must be affected to produce coma?
Consciousness is maintained by sensory stimuli passing through the ascending reticular activating system (ARAS) from the rostral brainstem to the cerebral cortex. Decreased consciousness results from global lesions of both central hemispheres or a lesion affecting the ARAS.
3. How does coma change emergency management?
With any emergency, ensuring a patent airway, providing adequate ventilation, and restoring circulating blood volume are necessary to prevent irreversible organ damage. The danger with animals suffering coma from increased intracranial pressure is that any therapeutic maneuver or drugs that increase brain blood volume may lead to irreversible brainstem herniation. In administering fluids and analgesics and in handling such patients, care must be taken to prevent iatrogenic increases in intracranial pressure.
4. Describe the initial treatment of comatose patients.
1. Check for a patent airway and ensure that ventilation is adequate. The partial pressure of carbon dioxide in arterial blood (PaCO2) should be kept below 35 mmHg to reduce cerebral blood flow and minimize cerebral edema.
2. Ensure adequate perfusion and cardiovascular function. Fluid therapy should be individualized because supernormal blood volume and pressure contribute to increased intracranial pressure.
3. Elevate the head and avoid compressing the jugular veins with catheters, bandages, or positioning.
4. Maintain body temperature between 99°F and 102°F.
6. Supply glucose as needed to maintain blood levels between 100 and 200 mg / dl.
7. Supplemental oxygen is important to ensure that the partial pressure of oxygen in arterial blood (PaO2) is above 60 mmHg. To avoid handling the animal’s head, an oxygen cage is preferable to face mask or nasal insufflation. Supplemental oxygen is not a substitute for ventilatory support and does not prevent hypercarbia. If the animal becomes hypercarbic, ventilatory support may be necessary to prevent increased intracranial pressure.
5. How does a history of trauma affect emergency management of coma?
Trauma causes structural damage to the brain through contusion, laceration, and hemorrhage. The presence of hemorrhage within the calvarium complicates therapy because aggressive fluid administration and oncotic agents such as mannitol may worsen intracranial hemorrhage. Patients with head trauma should be evaluated carefully for signs of focal neurologic deficits, which may indicate a space-occupying hemorrhage. The therapeutic goals in cases of head trauma include normalizing blood pressure by carefully titrating crystalloid fluid therapy; and maintaining tissue oxygenation through supplemental oxygen. Hyperventilation of head trauma patients is no longer recommended as the reduced blood flow may worsen ischemic injury.
6. When should mannitol be used in patients with increased intracranial pressure? What are the contraindications?
Mannitol, an osmotic diuretic, dehydrates tissues and is effective in reducing brain tissue volume. In the presence of diffuse cerebral edema, it is the most effective agent to decrease intracranial hypertension. Its effects depend on an intact blood-brain barrier. Mannitol may cause a dramatic elevation in intracranial pressure before it exerts its action and reduces tissue volume. Mannitol is contraindicated in patients with hypovolemic shock, active bleeding, or cardiovascular compromise. It may lead to volume overload and continued hemorrhage. If mannitol leaks into tissues, it may draw excessive fluids with it. This is a major concern with space-occupying intracranial hemorrhage. Mannitol may leak into the hematoma, bringing with it more fluid and further compressing the cerebrum.
7. What are the general pathophysiologic categories of coma?
• Bilateral, diffuse cerebral disease
• Compression of the rostral brainstem (midbrain, pons)
• Destructive lesions of the rostral brainstem
• Metabolic or toxic encephalopathies
8. Describe the diagnostic approach to comatose patients.
Potential brain disease first should be classified according to location of the lesion and clinical course over time. History, physical examination, and serial neurologic examinations are the most useful tools. The clinician should assume increased intracranial pressure (ICP) in any animal with altered consciousness. Care should be taken to avoid anything that would further increase intracranial pressure. Neurologic examination of the comatose patient should determine whether the lesion is focal, multifocal, or diffuse. The examination should be repeated frequently to determine whether the patient is improving, unchanged, or worsening. Primary central nervous system (CNS) disease causing coma and stupor should be considered when lateralizing signs or cranial nerve deficits are noted. Generalized disease of the cortex, cerebellum, or brainstem suggests a primary process outside the central nervous system. Diagnostic tests to look for evidence of toxic or metabolic disease or organ dysfunction help to differentiate primary CNS disease from other causes.
9. What initial laboratory evaluations should be performed in comatose patients?
Acute coma without a history of trauma suggests a toxic or metabolic disorder. Owners should be questioned about access to various drugs and poisons, including antidepressants, tranquilizers, alcohol, and ethylene glycol. Blood should be drawn immediately for serum chemistries, looking for evidence of organ dysfunction. Blood glucose can be tested easily on admission. Hypoglycemia may be treated quickly while its cause is investigated. A complete blood count may reveal signs of systemic infectious disease or thrombocytopenia. Urinalysis may reveal calcium oxalate crystals in cases of ethylene glycol intoxication, ammonium biurate crystals with hepatic insufficiency or casts and isosthenuria with acute renal failure. Activated clotting time (ACT) can be tested quickly to assess the intrinsic and common coagulation pathways; ACT is markedly prolonged in patients with acquired coagulopathies. Once the results of the screening tests have ruled out organ dysfunction and metabolic disease, cerebral spinal fluid analysis and either computed tomography or magnetic resonance imaging should be performed.
10. What are the major causes of coma?
|Intracranial mass lesions||Diabetic mellitus|
|Granulomatous meningoencephalitis||Ethylene glycol|
|Bacterial and fungal meningitis||Lead|
|Protozoal infections||Carbon monoxide|
11. Describe changes in pupil size, position, and reaction to light that help to determine location and severity of disease.
Symmetric pupils with normal direct and consensual response to light require a functional ventrorostral brainstem, optic chiasm, optic nerves, and retinas. Increased intracranial pressure and hemiation of the cerebellum under the tentorium cerebelli stimulate the nuclei of the oculomotor (third cranial) nerve, causing brief miosis of both pupils. As the pressure increases and the nuclei are irreversibly damaged, the pupils become fixed and dilated.
Anisocoria suggests primary CNS disease. If the pupils are unequal at rest but both respond normally to light and darkness, a unilateral cerebrocortical lesion contralateral to the larger pupil is likely. If the dilated pupil does not respond to light or darkness, a unilateral oculomotor nerve III lesion is present.
Metabolic diseases may cause symmetric miosis, whereas increased sympathetic tone may cause symmetric mydriasis. However, both respond normally to light and darkness. Symmetric miosis with no response to light or darkness is seen with damage to the pons, iridospasm, or bilateral sympathetic denervation (Homer’s syndrome).
12. What abnormal breathing patterns may be seen in comatose patients?
Lesions of the medulla may damage the basic rhythmic control of inspiration and expiration. Functional transection of the brainstem cranial to the medulla allows ventilation to continue but in gasps rather than smooth inspiration and expiration. Damage to the midpons cranial to the apneustic area results in apneustic respiration, characterized by prolonged inspiration and short expiration. Cheyne-Stokes respiration is characterized by deep breathing followed by periods of apnea or shallow respirations and indicates that normal feedback mechanisms no longer function. With normal control of ventilation impaired, the deep breathing causes a drop in CO2 of arterial blood. This drop is detected by the respiratory center in the brainstem, and respiration is inhibited. Progressive deterioration or compression of the brainstem often causes a slowing of respirations associated with rapid progression toward death.
13. What is the oculovestibular reflex? How can it be used to assess comatose patients?
Infusion of cold water into an ear canal normally induces horizontal nystagmus with the fast phase opposite the direction of the infused ear. Infusion of warm water induces horizontal nystagmus with the fast phase toward the infused ear. This caloric test of the oculovestibular reflex requires integrity of the brainstem, medial longitudinal fasciculus, and cranial nerves III, IV, VI, and VIII.
14. What is hepatic encephalopathy?
Hepatic encephalopathy is a clinical syndrome characterized by abnormal mentation, altered consciousness, and impaired neurologic function in patients with advanced liver disease and severe portosystemic vascular shunts. Hepatic encephalopathy results when the liver fails to remove toxic products of gut metabolism from the portal blood. Ammonia, mercaptans, short-chain fatty acids, and gamma-aminobutyric acid (GABA) agonists have been implicated in the pathogenesis of hepatic encephalopathy.
15. How is hepatic encephalopathy diagnosed?
Hepatic encephalopathy is suspected in patients with bizarre behavior after eating or with altered mentation and elevated liver enzymes. With hepatocellular damage both alanine transferase (ALT) and aspartate transferase (AST) are elevated. With congenital portosystemic shunts or end-stage liver failure, ALT and AST may be normal. Chemical parameters that suggest poor liver function include low blood urea nitrogen, low blood glucose, low albumin, lower serum cholesterol, and elevated serum bilirubin. Fasting and postprandial serum bile acids are markedly abnormal. Blood ammonia levels may be normal or elevated. Nuclear scintigraphy may be used to quantitate blood flow around the liver with portosystemic shunts.
16. What treatments are available for patients with hepatic encephalopathy?
Withdrawal of dietary protein is necessary to prevent production of intestinal ammonia. A 10% povidone iodine enema solution rapidly suppresses colonic bacteria and impairs ammonia production. Lactulose (1-4-beta-galactosidofructose; Cephulac, Merrell-Dow) is hydrolyzed by intestinal bacteria to lactic, acetic, and formic acid. With the lower intestinal pH, ammonia (NH3) accepts an additional H+ proton to form the less diffusible ammonium ion (NH4), effectively trapping ammonium within the colon. Lactulose is an unabsorbed solute and also causes an osmotic diarrhea, decreasing intestinal transit time and absorption. Lactulose may be given orally but should be given rectally in patients with altered mentation. Patients with chronic intractable portosystemic encephalopathies may benefit from the benzodiazepine antagonist flumazenil.