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Vital sign level of consciousness

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Causes and Treatments of Coma

 

Since one cannot question the patient, other avenues for history are utilized. Medical tags and bracelets are sought. The questioning of EMTs is vital. Were empty medicine bottles present in the house? If so, they should be brought to the emergency department. Family and friends and neighbors and bystanders should be questioned. A handy mnemonic device for remembering the multiple causes of coma is “TIPS” and “AEIOU”.
Treatment for coma is supportive until the cause is found. The ABC’s of resuscitation are strictly followed.

"TIPS”:

Trauma, Temperature

Trauma: in addition to head trauma, shock from hemorrhage, pericardial tamponade, myocardial contusion and tension pneumothorax may cause a decreased level of consciousness. A concussion is a transient loss of consciousness with no brain damage. A contusion, or bruising of the brain with small hemorrhages and tissue tears, usually causes a loss of consciousness, sometimes briefly, sometimes for a long period (diffuse axonal injury). A traumatic subarachnoid hemorrhage from injury to vessels in the pia causes bleeding into cerebrospinal fluid in the subarachnoid space, sometimes producing headache and stiff neck. An epidural hematoma is a collection of blood between bone and dura from a laceration of the middle meningeal artery. A subdural hematoma is blood between the dura and arachnoid from tears in bridging dural veins. An intracerebral hemorrhage is the accumulation of blood within brain substance. A CT will not show concussions or in many cases contusions, but does reveal epidural, subdural and intracerebral hemorrhages.
Treatment: increased intracranial pressure (ICP) is treated as previously described. Epidural and subdural hematomas require surgical evacuation.

Temperature: This can include hypo- and hyperthermia.

Infection
Common infections causing decreased levels of consciousness are sepsis and bacterial meningitis (viral meningitis usually does not cause coma, except in the pediatric population). Neurological findings in sepsis range from lethargy or agitation to coma. Inflammatory mediators cause multi- organ-system failure and hypotension (septic shock) with inadequate perfusion to the brain. Bacterial meningitis is seen primarily in pediatrics and the elderly, with sporadic outbreaks in other populations. With the advent of the H. influenzae vaccine, the main organism is Strep. pneumoniae, not only in peds but in all age groups. Seeding is from bacteremia, otitis media and sinusitis. Fever, headache, altered mental status and HIV+ are important historical items. Seizures may occur. The physical exam in infants may show hypothermia, a bulging fontanelle, lethargy, dehydration and otitis media. Older children and adults usually have nuchal rigidity, pain on extension of the legs (Kernig sign) and passive neck flexion producing flexion of the hips (Brudzinski sign). In meningococcal meningitis the skin may show petechiae and purpura.
Treatment: when meningitis is suspected, IV antibiotic therapy (ceftriaxone or cefotaxime 2 gm, 50mg/kg in peds) is begun before lumbar puncture. The presence of papilledema and loss of spontaneous venous pulsations indicate increased intracranial pressure, and therapy for ICP should be begun immediately (see earlier section). When ICP is suspected, a CT should be done before an LP.

Stroke, Shock, Seizures
A patient with a cortical ischemic stroke involving one side of the brain, with a profound sensory and motor loss on the opposite side of the body along with aphasia (left brain) or inattention and unconcern (right brain) and sometimes confusion, experiences no loss of consciousness unless massive ischemia causes brain edema. The less common brainstem ischemic stroke (basal artery) causes coma from involvement of the RAS (see earlier section). A hemorrhagic stroke begins with a headache and alteration in consciousness that progresses to coma because of a severe global mass effect with increased intracranial pressure, compression of the brainstem and herniation. Diagnosis is made by CT.
Treatment:
1. The ABCs are followed;
2. Blood pressure over 220/120 is treated with increments of labetalol 20 mg IV;
3. Increased intracranial pressure is controlled;
4. Neurosurgical consultation is obtained and
5. The thrombolytic t-PA 0.9mg/kg IV (maximum 90mg) may be given over an hour for an ischemic stroke if the time of onset is known to be less than three hours (and no contraindications exist).

A subarachnoid hemorrhage is caused by rupture of a congenital (berry) aneurysm in the Circle of Willis at the base of the brain, either at rest or during exercise. The patient describes a sudden severe headache. Bleeding into the subarachnoid space and ventricles produces a mild to severe decrease in level of consciousness. Preliminary diagnosis by CT or lumbar puncture may be supplemented by angiography.
Treatment:
1. Blood pressure is controlled by labetalol 20mg IV increments in pre-hemorrhage levels;
2. The calcium-channel blocking agent nimodipine 60mg PO every 6 hours reduces vasospasm;
3. Seizures are prevented with fosphenytoin (cerebyx) 15mg/kg IV as a loading dose and
4. Neurosurgical consultation is obtained.

Seizures: the most common cause of a seizure is failure to take anticonvulsive medicine. Decreased level of consciousness is transient and the person gradually awakens (post-ictal state). A rapid blood sugar is checked and glucose is administered as needed. if the sezure continues, it is stopped with lorazepam (Ativan) 4 mg IV over 2 minutes (Peds: 0.1 mg/kg) (or midazolam ((Versed)) 0.2 mg/kg IM). For the persistent seizure (status epilepticus), a second dose of fosphenytoin (Cerebyx) 20 mg/kg IV. If no response occurs, phenobarbitol 18 mg/kg IV is used, and intubation may be required. The continuous seizure may require a neuromuscular blocking agent (i.e., vecuroium 0.1 mg/kg) or general anesthesia. Other causes of seizures are congenital/genetic disorders, brain tumors, eclampsia, drugs such as theophylline, phenothiazines, lithium, cocaine and antidepressants, opportunistic cerebral infections in AIDS patients and febrile seizures.

"AEIOU”:

Alcohol/Drugs

Alcohol: wide variability exists in each person’s response to alcohol, depending on whether one is a chronic alcoholic or an occasional drinker. This results in various degrees of intoxication, physical dependency (withdrawal symptoms on stopping the drug) and tolerance (increased amounts of drug for the same effect). In the emergency setting, it is not uncommon to see an alert and oriented alcoholic with a blood alcohol level of 400 mg/dL, while a nonalcoholic may be comatose at that level. A level of 100 mg/dL is legal intoxication in most states. The nontolerant person usually shows a decrease in level of consciousness at a level of about 300 mg/dL. Coma (GCS of 8) may occur at about 400 mg/dL (often requiring intubation), and death from respiratory depression may occur at 500 mg/dL (LD-50).
The alcoholic is at increased risk for a subdural hematoma, and a search for bruises and abrasions should be sought. A rectal temperature is required. A low threshold should exist for a head CT, as well as a diagnostic peritoneal lavage to rule out abdominal injuries. Labs should include, in addition to a serum ethanol level, a drug screen (cocaine is a common accompanying drug) and a serum ammonia to rule out hepatic encephalopathy. Alcohol withdrawal is seen about 48 hours after the last drink and exhibits a wide variety of manifestations, including anxiety, tremors, visual hallucinations and seizures, but usually does not show a decreased level of consciousness. Withdrawal may be seen in the intoxicated patient.
Treatment for alcohol withdrawal:
one liter of D5NS with MgSO4 2 gm, folate 1 mg and an ampule of multivitamins is administered for both intoxication and withdrawal since glycogen, magnesium and vitamins are usually depleted. Gastric decontamination with lavage and charcoal is indicated only in the rare case of an acute ingestion of a large amount of alcohol over a short period of time in a nonalcoholic. For withdrawal, lorazepam (Ativan) 2-4 mg IV is administered, followed by 2 mg every 30 minutes as needed.

The alcoholic may present with liver failure and coma from hepatic encephalopathy, a condition in which nitrogenous and other compounds (i.e., ammonia, gamma-aminobutyric acid, mercaptans) normally removed by the liver accumulate and gain access to the central nervous system, causing neuroinhibition and cerebral edema. The serum ammonia is elevated, electrolytes are often abnormal and asterixis (“liver flap” = hand tremor) is sometimes present.
Treatment for hepatic encephalopathy: fluid and electrolyte abnormalities are corrected. Lactulose may be given via nasogastric tube (30 cc TID). Lactulose is a nonabsorbable disaccharide when in contact with colonic bacteria traps ammonia in the colon as nondiffusible ammonium ions. Neomycin (1 gm via NG q8h) suppresses bacteria responsible for the production of ammonia and other nitrogenous compounds.

Drugs: it is not appropriate to list the multitude of drugs and toxins that may cause an altered level of consciousness. Common drugs causing coma are sedative/hypnotics and narcotics. An altered level of consciousness is seen occasionally with carbon monoxide poisoning. Narcotics (i.e., morphine, heroin) bind to opioid receptors in the brain (mu receptors). Sedativehypnotics (alcohol, benzodiazepines and barbiturates) facilitate gammaaminobutyric acid (GABA), the major inhibitory neurotransmitter of the central nervous system. Benzodiazepines and barbiturates bind to GABA receptors. No receptor has been identified for alcohol, but alcohol enhances the action of GABA receptors.
Treatment: the treatment for an overdose of a sedative/hypnotic or narcotic is gastric lavage within the first hour. After the first hour activated charcoal 50 gm PO or by gastric tube is administered to prevent absorption of the drug. If the gag reflex is lost, the patient is intubated and gastric lavage and/or charcoal is administered by gastric tube. The antidote for opiate ingestion is naloxone, a competitive antagonist at the mu opioid receptor site. The person awakens quickly. Naloxone may then be administered 1 mg in 250 cc NS at 250 cc per hour. Flumazenil (Romazicon) 0.2 mg IV is a competitive antagonist of the benzodiazepine receptor and will reverse a benzodiazepine overdose. However, since seizures have been reported with Flumazenil, it should be used for diagnostic rather than therapeutic purposes.

A common inhalation injury is carbon monoxide poisoning from fires, faulty gas heaters and in machine-shops where ventilation is poor. Carbon monoxide (CO) is odorless and binds to hemoglobin 210 times more readily than oxygen. Early symptoms are headache, dizziness, weakness and nausea. Consciousness is affected at CO levels of 20-30%, confusion and syncope occur at 40%, coma and seizures take place at 50%, and death occurs at 60%.
Treatment: 100% oxygen by nonrebreather mask until the level is 0. Use of hyperbaric oxygen therapy (HBO) is controversial, but is indicated for comatose patients, those with major illnesses such as coronary artery disease and the pregnant patient.

Endocrine, Electrolytes

Endocrine: severe hypothyroidism (myxedema coma) and acute adrenal insufficiency (from an exacerbation of Addison’s disease) are occasional endocrine causes of decreased level of consciousness. Signs of myxedema are hypothermia (75%), obesity, a surgical neck scar, cool dry skin, delayed DTRs, anemia, electrolyte disturbances, and occasionally respiratory distress, bradycardia and CHF. Acute adrenal insufficiency is sometimes seen when steroids are withdrawn in a patient with Addison’s disease. Patients present with confusion, lethargy, nausea, vomiting, hyperpigmentation and hypotension. Lab studies show hyperkalemia, hyponatremia and hypoglycemia.
Treatment: hydrocortisone 100 mg and 2 liters of D5NS to restore blood pressure and correct hypoglycemia. Hyperkalemia is treated with an ampule of bicarbonate over 5 minutes. If the K+ level is >8 meq, 10 cc of a 10% calcium gluconate solution is administered over 10 minutes.

Electrolyte imbalances rarely cause a decrease in level of consciousness. Occasionally severe hyponatremia may cause decreased mentation from the syndrome of inappropriate antidiuretic hormone (SIADH) secretion from a previous intracranial lesion or tumor.
Treatment: water restriction. For severe hyponatremia (< 115 mEq), 3% saline is administered at 100 cc per h.

Insulin

The most common disorder causing an altered and/or decreased level of consciousness in all categories is hypoglycemia (glucose level < 50 mg) in the insulin-dependent diabetic patient with decreased food intake (insulin reaction) or the occasional patient on oral medication. Confusion is present, and if sustained for any length of time a decreased level of consciousness occurs.
Treatment: IV glucose (D50) quickly reverses the condition. If an IV is difficult to obtain, glucagon 1-2 mg may be administered IM (glucagons catabolizes stored glycogen). Diabetic ketoacidosis (DKA), indicated by glucose >250 mg, bicarb <15 mEq and pH <7.3, is treated with normal saline, 5 L at 500 cc per hour, insulin 0.2 units/kg initially, then 0.1 unit/kg/ h IV infusion, potassium 20 mEq per liter and bicarbonate 1 to 2 amps if pH is <6.9. The patient with hyperosmolar hyperglycemic nonketotic coma (HHNC) (glucose >600 mg, negative ketoacidosis) is lethargic and confused but rarely comatose. Fluid and potassium treatment is similar to DKA, except that less insulin and more fluid is required.

Oxygen
Oxygen deficits are discussed in Chapter 4. An insidious cause of decreased mentation is hypercapnia (carbon-dioxide narcosis) from hypoventilation from many causes: two common ones are acute pulmonary edema and a tiring asthmatic. The pCO2 level in these cases is elevated above 50 mmHg (sometimes to 100 mmHg) and the pH is decreased (respiratory acidosis). Pulse oximetry may show a normal oxygen saturation.
Treatment: increased ventilatory support, requiring intubation and mechanical ventilation.

Uremia
Uremia (chronic renal failure) is caused by the accumulation of toxic products of protein metabolism in the bloodstream. The blood urea nitrogen (BUN) and creatinine are increased. An altered mental status is believed to be related to loss of the kidney’s capacity to synthesize vitamin D, leading to hypocalcemia and secondary hyperparathyroidism. Definitive treatment is dialysis.

 


 
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