1. Neurological-Cerebral and Cognitive Health Systems

Overview

The neurological-cerebral health system is concerned with the body's ability to receive and respond to stimuli. This health system includes the functions of the brain and the nerves and the structures that support these. The neurological-cerebral health system review includes assessment of level of consciousness as well as mental status. Mental status is usually assessed through characteristics of speech, nature of thought processes, general behavior and appearance, orientation, and memory. Patients with primary motor sensory deficits related to disruption of the peripheral nervous system are evaluated in this health system as well as in the sensory health system. In addition, patients with functional psychoses such as delirium or schizophrenia may be classified as having an alteration in neurological-cerebral health. The cognitive health system addresses the individual's ability to process and transmit information based on developmental, educational, and physiological capabilities.

Cue Words

RELATED NURSING DIAGNOSES

Neurological-Cerebral Health System

sensory perceptual alteration (specify)
sleep pattern disturbance
altered thought processes
potential for injury
dysreflexia

Cognitive Health System

knowledge deficit
altered growth and development
decisional conflict
impaired verbal communication
altered thought processes
potential for injury

Department of Emergency Medicine Triage Protocols

Case Studies

1.1 MIGRAINE HEADACHES

Cynthia A. Kaczmarek, RN, BSN

Barbara is a 35-year-old black female who comes to the emergency department (ED) with a severe headache that has lasted over 4 days. At triage, Barbara appears to be in acute distress. Unable to find a comfortable position, she is holding her head in her hands while rocking back and forth. Barbara's vital signs on arrival are temperature 98.6° F, pulse 90. respirations 28. and blood pressure (BP) 214/129. Barbara describes paresthesia on the right side of her body with some tingling and weakness in the right hand. She has a right facial droop. Barbara also complains of having had nausea and vomiting for this same 4-day period.

Triage Assessment, Acuity Level IV: Appears in acute distress, describes "worst headache. " BP diastolic >l 15, and neurological deficits.

Barbara is brought immediately to the treatment area where she describes visual changes with streaking, flashing lines that began with the onset of her headache. Barbara states that her menses just finished prior to the onset of this attack, a usual precursor for her headache. Barbara also shares that she has been feeling "depressed" since she separated from her husband 2 months ago. Barbara's past medical history includes diagnosed migraine headaches with almost monthly visits to the ED. Hypertension and depression are also chronic problems for her.

Barbara's current medications include hydrochlorothiazide (HCTZ), verapamil, nortriptyline, Reglan, Phenergan, and Demerol. She is allergic to Compazine (seizures), Stadoi and Thorazine (syncope), Inderal (rash), codeine and Dilaudid (nausea). Barbara's physical assessment is normal except for the described neurological dysfunctions.

Barbara is placed in a room that is darkened and away from the main flow of activity. She is started on an intravenous solution of normal saline at 250 ml/hr. While in the ED. Barbara receives a total of 450 mg of meperidine with 150 mg of Vistaril, all given intramuscularly, before any relief of her headache and symptoms is obtained. When Barbara is released from the ED. no prescriptions are given to her and she is instructed to have a follow-up with her private neurologist.

QUESTIONS AND ANSWERS

1. What are migraine headaches?

   Headaches are one of the most common ailments affecting people in the United States. Approximately 20% of the population experiences a type of headache that can be classified as a migraine. Most migraine conditions begin in adolescence and affect females twice as often as males (1,2). Research suggests that there is a family history associated with migraines.

   The exact cause of migraines is still unknown. It is believed that migraines are of vascular origin affecting both the intracranial and, extracranial arteries (2). A study done by Graham and Wolff in the late 1930s suggests that an unidentified substance causes a cascade of events that may include platelet aggregation and release of various substances such as platelets, serotonin, and kinins (1, 3). A symptomatic vasoconstriction occurs in response to these substances and is usually focal. This vasoconstriction is followed by a reactive vasodilation in the extracranial arteries which results in the throbbing pain that is associated with the migraine headache (1).

   There are two types of migraine headaches: classic and common. Classic migraines occur in approximately 10% of patients with migraines. In most cases there is a prodromal phase which begins about 30 min prior to the actual headache. In this prodromal phase there is usually some sensory dysfunctions such as visual deficits. scatomas, tingling, and paresthesia (2). The headache usually has a rapid onset with pain that is unilateral. The pain tends to concentrate in the frontal region and may radiate. Patients often describe the pain as throbbing and in synchrony with their pulse (3). Some accompanying symptoms include nausea and vomiting and an increase in BP. The headache can last anywhere from several hours to several days. As this description would suggest, Barbara experiences classic migraine headaches. The neurological findings with Barbara's headaches such as the facial droop and tingling in the extremities can be associated with her high BP and the many pontine hemorrhage scars that have been found on CAT scans of her brain.

   The common migraine headache features many of the same symptoms of the classic migraine. However, the prodromal phase is not as severe. The common migraine headache can produce many of the accompanying symptoms such as nausea and vomiting lasting for several hours to several days(3).
   
   

2. How is the diagnosis of migraine headache achieved?

   The diagnosis of migraine headache is based largely on the patient's history and presentation. The physical exam is usually unremarkable (4). Lab studies are usually not helpful. Sometimes, as in the case of Barbara, a CAT scan will reveal hemorrhages that have occurred as the result of high BP or excessive vasodilation of the arterioles.

   Important facts for the nurse to include in the assessment of the patient include when the headache began; any predisposing factors that the patient can relate to the onset of the headache such as stress, menses. or family crisis; and the duration and the quality of the pain. It is clear from Barbara's history that many of these factors are present for her. The patient should also be asked if any measures taken have been effective in helping to reduce the pain. The nurse also needs to be aware of the patient's BP as a possible cause for the neurological changes that the patient is experiencing.
   
   

3. What nursing diagnoses should be considered in this patient presentation?

   Many different factors need to be assessed when identifying nursing diagnoses for the migraine patient. The patient presents because there is significant pain. The patient's nutritional status and complications of nausea and vomiting that accompany migraines should be considered. Social, environmental, and psychological factors that may have an effect on the patient also should be assessed.

   Diagnosis: Pain related to reaction vasodilation of extracranial arteries associated with migraine headache
   Desired patient outcome: The patient will state that there has been a reduction in pain; the patient will exhibit behavioral cues that are consistent with the relief of pain such as no more rocking or head holding.

   Diagnosis: Diagnosis: Fluid volume deficit related to nausea and vomiting
   Desired patient outcome: The patient will take 2000 ml of fluids intravenously or orally; the patient will not experience orthostatic vital sign changes; the patient's skin turgor will improve, mucous membranes will be moist.

   Diagnosis: Altered cerebral perfusion related to high BP and migraine phenomena
   Desired patient outcome: The patient will have a reduction in BP of less than 100 mg Hg diastolic; the patient will describe resolution of the numbness and tingling of right hand; facial droop will resolve.

   Diagnosis: Ineffective individual coping related to personal vulnerability in a situational crisis
   Desired patient outcome: The patient will be able to identify personal strengths that may promote effective coping: the patient will state a plan for either accepting or changing the situation: the patient will be able to identify and access community resources that are available when she feels unable to cope.
   
   

4. What are the medical and nursing care measures for the patient with a migraine headache?

   The care provided to Barbara is useful in the management of any patient with a migraine headache. The patient needs to be placed in a darkened room that is away from the center of activity, and disturbed as little as possible. Decreasing the neurological and sensory stimulation to the patient helps in reducing the intensity of the pain associated with the migraine headache. Vital signs, especially BP. should be monitored. Barbara's BP is significantly high and she is having pronounced neurological changes. A stroke may occur because of the high pressure. A patient, like Barbara, should be assessed for deterioration of neurological signs that may include a decreased level of consciousness, alterations in speech patterns, pupillary changes, and other signs associated with cerebral vascular accidents. For the patient with a migraine headache a rapid reduction in BP may help to alleviate these symptoms. The patient should be given antiemetics such as Compazine or Phenergan to help relieve some of the accompanying symptoms of nausea and vomiting. Since Barbara is allergic to Compazine, she was given Phenergan. Fluids should also be provided, either intravenously or by mouth.

   Pain medications should be administered as ordered. Narcotic analgesics are usually not recommended in the management of migraines. Because of the frequency of migraine attacks with some patients, the continual use of narcotics for pain management may cause the patient to become narcotic dependent or tolerant. However, if the attack is intractable, then narcotic analgesia may be required (5).

   One of the most widely used drugs for the treatment of migraines is ergotamine. It is believed that this drug works by constricting the already dilated cranial arteries (5). For best results, this drug needs to be taken not more than 30 min after the prodromal phase begins (5. 6). Ergotamine had been tried for Barbara in the past but did not work for several reasons. A side effect of ergotamine therapy is an elevation of BP that could ultimately result in decreased arterial blood flow and tissue ischemia (6). Also, if the patient experiences a migraine headache more than twice a month, a different form of therapy is usually recommended. Since Barbara has chronic hypertension and often has frequent migraine attacks, it was decided that this would not be a beneficial treatment for her.

   A prophylactic treatment plan needs to be initiated if the patient experiences migraines more than twice a month. This plan includes a visit and follow-up appointments with one doctor, preferably a neurologist. With this plan of treatment the patient works with the doctor on a one-to-one basis to try to establish a treatment plan of medications that works best for the individual patient and thereby decreases the number of ED visits and provides for consistency in care when an ED visit is needed.

   Calcium channel blockers such as verapamil have in recent years been shown to be effective in the management of the migraine patient by increasing blood flow and oxygen supply to the tissues (6). Antidepressants such as the tricyclic antidepressants Elavil and Amitril have also been shown to be useful in long-term care (6). Antidepressants have sedative actions. They also increase the serotonin uptake from the synapses (6) which is believed to play a role in the cause of migraines. These drugs are still under investigation for use as treatment for migraines.

   Barbara is well known to the ED staff. Her treatment plan for her depression usually involves talking with the ED psychiatrist and trying to identify resources within herself and her community that can help her cope more effectively. Barbara was referred back to her community psychiatry program for ongoing help in managing her most recent personal crisis following discharge from the ED.

REFERENCES

1. Diamond S. Migraine headache: Working for the best outcome. Postgrad Med 81:174,1987
   
   
2. Lewis SM. Collier 1C: Medical-surgical nursing: assessment and management of clinical problems. New York: McGraw Hill, 1418, 1983.
   
   
3. Sandier M: Monoammes and migraine: a path through the woods. In: Diamond S, Dalessio D. Graham J. et al., eds. Vasoactive substances relevant to migraine. Springfield, IL: Charles C Thomas. 3-18, 1975.
   
   
4. Gunderson CH: Management of the migraine. Am Fam Phys 33:138-139. 1986.
   
   
5. Edmeads JG: Migraine. Can Med Assoc J 138:107-109, 1988.
   
   
6. Govoni LE, Hayes JE: Drugs and nursing implications. 5th ed. Norwalk. CT: Appleton-Century -Crofts. 66-67. 509, 1269, 1985.
   
   
7. Kim M, McFarland G. McLane A: Pocket guide to nursing diagnoses. St. Louis, C. V.  Mosby, 1984.

1.2 SEIZURES: WHEN ALCOHOL IS THE CULPRIT

Kathleen J. Barnett, RN, MSN, CEN

Mr. H. is a 44-year-old white male who arrives in the ED after experiencing a generalized tonoclonic seizure at home, witnessed by his fiancée. The seizure occurred approximately 1 hr prior to arrival. Mr. H admits to a long history of alcohol (ethanol) abuse and has experienced previous withdrawal seizures, although he denies any history of delirium tremens or blackouts. He was previously on phenytoin, but has not been on it "for a long time. " Mr. H. states he drank 4 quarts of beer the previous evening. He is anxious and tremulous, and ambulates with a cane. Vital signs at triage are BP 170/100, pulse 112, respirations 28, and temperature 37.6°C (99.6°F). Mr. H. is oriented to person, place, and time. but does not recall the President of the United States or other significant current events. Strength, sensation. and cranial nerves are intact, and reflexes are normal. However. Mr. H. has severe gait ataxia and minimal end-gaze nystagmus. Finger-to-nose coordination is slightly dysmetric. Sclera arc injected, and there are significant dental caries. The neck is supple and lungs are dear: heart sounds reveal an S4 gallop. The abdomen is soft and non-tender, with no masses or organomegaly. .Mr. H. denies any illicit drug use, but smokes two packs of cigarettes a day.

Triage Assessment, Acuity Level III: Recent seizure activity and recent ethanol ingestion with history of alcohol withdrawal seizures: tremors; ataxia.

When Mr. H. is brought to the treatment area, a 1000 ml solution of 5% dextrose and 0.45% normal saline is started at 125 ml/hr with additives of 1000 mg thiamine, 0.2 mg folic acid, and 2 g magnesium sulfate. Labwork is drawn simultaneously for a complete blood count (CBC), differential, electrolytes, calcium, magnesium, amylase, bilirubin, prothrombin time (PT), partial thromboplastin time (PTT), and ethanol level. Mr. H. is placed on a stretcher with side rails up in a well-lighted, high-observation area of the ED. A vest restraint is applied.

QUESTIONS AND ANSWERS

1. What nursing diagnoses are applicable to this patient?

   The patient with chronic alcohol abuse, alcohol withdrawal, or alcohol intoxication has a multitude of problems due to the multi-systemic effects of the drug, including psychosocial complications. Obviously, not all nursing diagnoses can be addressed in the ED visit; however, the following diagnoses would likely be high on the priority list for the patient experiencing alcohol intoxication or withdrawal manifested by seizure activity.

   Diagnosis: Potential for injury related to seizures or to altered sen-sorium secondary to alcohol intoxication
   Desired patient outcome: The patient will be seizure-free. If seizures recur, patient is in a safe environment that will protect him from falls or other injury.

   Diagnosis: Fluid volume deficit related to ethanol-induced diuresis and/or decreased fluid intake
   Desired patient outcome: The patient maintains a heart rate less than 100 beats/min and systolic BP greater than 90 mm He. Urine output remains at greater than 30 ml/hr. Mucous membranes are moist.

   Diagnosis: Altered nutrition, less than body requirements, related to diminished dietary intake, diminished absorption of nutrients, and/or nonnutrient caloric intake
   Desired patient outcome: Patient demonstrates improved nutritional status as indicated by appropriate lab values, particularly glucose, ketones, and magnesium.

   Diagnosis: Alteration In sensory-perceptual pattern related to central nervous system (CNS) depressant effects of ethanol or to hallucinations
   Desired patient outcome: The patient will remain free of hallucinations or experience a reduction or cessation of hallucinations. if occurring. The patient will be alert and oriented.

   Diagnosis: Knowledge deficit of effects of alcohol on the body
   Desired patient outcome: Patient is able to describe the relationship between alcohol and his symptoms, verbalize ways in which some deleterious effects might be avoided, and state where he can be referred for detoxification.
   
   

2. What is the basis for Mr. H.'s seizure and other neurological symptoms?

   A seizure is the sudden, recurrent transient disturbance in mental status, body movement, or both caused by excessive electrical discharges of brain cells. A seizure disorder is a symptom, not a disease. Mr. H's symptomatology is related to the adverse effects of chronic ethanol abuse, recent excesses, and acute withdrawal. Alcoholism is defined as the continuing of drinking despite physical, social, or occupational problems related to alcohol use.

   After ethanol is ingested, it is primarily absorbed in the lumen of the small intestine, although a small amount is absorbed through the gastric mucosa. Numerous factors influence the rate of ethanol absorption, including the concentration of ethanol in the beverage. pH and buffering capacities of the beverage, concentrations of congeners (chemical components that affect color, taste, and aroma) in the beverage, gastric emptying time following ingestion. emotional state of the drinker, and type and amount of food ingested with or before ethanol (1,2). Because ethanol is distributed throughout the body to all tissues based on their water content, persons with greater body mass or greater body water can ingest proportionately higher amounts of ethanol and still maintain lower intravascular and body tissue concentrations (1).

   More than 90% of ethanol ingested is metabolized in the liver. Only 2 to 10% is excreted by the lungs or kidneys, although the amount of ethanol in expired air or urine is directly proportional to the blood alcohol concentration (BAC) (1). The ability of the liver to metabolize ethanol may increase significantly with increasing amount and duration of ethanol ingestion, as the enzymes in the liver for alcohol and drug metabolism increase. Because of this phenomenon, other drugs may show accelerated clearance in the alcoholic as well, including anticoagulants. anticonvulsants. antibiotics, and oral antidiabetic agents.

   The alcohol withdrawal syndrome that occurs with patients who are alcoholics has been grouped into four stages of increasing severity (3). Although the patient in withdrawal does not necessarily go through all four stages, each stage has a distinct set of signs and symptoms that defines it.

   Stage one occurs at 6 to 8 hr following cessation of alcohol intake. It is characterized by mild tremulousness, anxiety, nausea, vomiting. and insomnia. The patient may be diaphoretic and easily startled. Tachycardia, mild hypertension, and hyperreflexia may also be present.

   In stage two, which usually begins at 24 hr after cessation or reduction of alcohol intake, the autonomic hyperactivity of stage one continues, but the patient experiences hallucinations. These are primarily auditory, but may also be visual, tactile, or olfactory.

   Stage three of alcohol withdrawal generally occurs at 7 to 48 hr after reduction or cessation, and is characterized by seizures. One or more seizures may occur over several hours: more than half of patients who develop withdrawal seizures experience multiple seizures (4), If untreated. the seizures may progress to delirium tremens.

   The onset of delirium tremens is the hallmark of stage four. Frequently seen 3 to 5 days after cessation or reduction of alcohol intake. delirium tremens are characterized by autonomic hyperactivity— tremors, diaphoresis, fever, hypertension, and tachycardia—and by illusions, hallucinations, and global confusion (3, 5).
   
   

3. How can it be determined that Mr. H.'s seizure is ethanol-related? Isn't it possible that idiopathic epilepsy, head trauma, or other drug toxicities could be the cause of the seizures?

   It is certainly possible that Mr. H.'s seizure could be due to any one of a number of etiologic factors or to a combination of factors. For instance, it is possible that Mr. H.'s drinking has suppressed an epileptic cause for his seizure that becomes apparent when drinking stops. Alcohol withdrawal seizures are a diagnosis of exclusion. Any first-time seizure should appropriately receive hospital admission and a diagnostic workup. However, a number of factors will assist in determining if a seizure fits the pattern of alcohol withdrawal.

   History of seizures and use of antiepileptic medications are indications of previous problems. The medical record should be referenced to confirm this. particularly if the patient is postictal or a poor historian. Mr. H. stated that he had taken phenytoin at an earlier time. Phenytoin may be given to a patient with ethanol withdrawal seizures, but only for a limited period as prophylaxis. The usefulness of phenytoin as a long-term maintenance therapy for the patient with alcohol withdrawal seizures has not been demonstrated (6). The major antiepileptic drugs are described in Table 1.2.1.

   Alcohol withdrawal seizures are usually grand mal seizures, but of shorter duration than idiopathic seizures (7). Tongue biting and loss of sphincter control are less common in alcohol withdrawal seizures than in idiopathic seizures (8). The electroencephalogram (EEG) of the patient experiencing an alcohol withdrawal seizure will return to normal after seizure activity, whereas the EEG of a patient experiencing an idiopathic seizure will display abnormalities during and following the seizure (8). Focal seizures are not associated with alcohol withdrawal and necessitate workup to rule out a space-occupying lesion resulting from head trauma or other pathology (9). A close examination of the head and neck should be performed to detect any external signs of trauma in a patient with seizures.

Table 1.2.1 Major antiepileptic drugs

4. What nursing interventions would be appropriate to initiate in this situation?

   Mr. H. presents with a history of alcohol withdrawal seizures, recent ingestion of alcohol, and a witnessed seizure prior to arrival. This combination of factors makes it apparent that Mr. H. continues to be at risk for further seizure activity. Mr. H. should be placed in a well-lighted, high observation area of the ED. Precautions should be taken to prevent injury to Mr. H. should another seizure occur—side rails should be up. padded, and stretcher wheels should be locked. Mr. H. should be placed on his side to allow drainage of secretions in the event of seizure, and airway equipment should be readily available. A vest restraint may be indicated for some patients, as seizure activity can be violent and bring a patient off a stretcher.

   The presence of tremors, ataxia. and anxiety, and the automatic hyperactivity demonstrated by hypertension and tachycardia all point to the need for sedation for Mr. H. Recognition of the signs and symptoms of alcohol withdrawal and prompt sedation of the patient will prevent worsening of symptoms and hopefully prevent further seizure activity. The benzodiazepines are generally recognized as the drug of choice for alcohol withdrawal symptoms, with chlordiazepoxide and diazepam the most commonly used agents. Intramuscular absorption of these two drugs is erratic and unreliable: therefore this route should be avoided. Oxazepam is available for oral administration and has a shorter half-life than either chlordiazepoxide or diazepam. Reassurance is also an important component in allaying the anxiety and fear that are associated with alcohol withdrawal.

   Vital-sign monitoring will be essential for Mr. H. All his vital-sign parameters are outside normal limits on his admission to the ED. Frequent monitoring will assist in determining if Mr. H. is returning to a normal baseline or if he is progressing further in the alcohol withdrawal syndrome.

   Initiation of intravenous hydration and supplementation of intravenous fluid with vitamins and magnesium are necessary. The chronic alcoholic not only faces the volume depletion caused by diuresis and inadequate fluid intake, but also malnutrition from diminished intake and absorption of protein, B vitamins (especially folic acid and thiamine). and certain minerals. Alcohol also increases urinary losses of amino acids, magnesium, potassium, and zinc. Administration of intravenous fluid with magnesium, thiamine. and folate or multivitamin additives should be standard therapy for the chronic alcoholic with withdrawal symptoms. Glucose should be given to any unconscious patient in the ED to rule out hypoglycemia: in the malnourished chronic alcoholic glucose provides carbohydrate calories as well.

TIP: Thiamine is a coenzyme in the metabolism of glucose, and should always be given prior to glucose in the chronic alcoholic patient to prevent precipitation of Wernicke-Korsakoff syndrome, which is manifested by oculomotor abnormalities, nystagmus, ataxia of gait, and global confusion. Thiamine can be safely given intra-venously either directly or by infusion in most intravenous solutions.

TIP: A finger stick (Dextrostix) blood glucose should be checked routinely on all patients who present with seizure. Seizures can cause hypoglycemia; hypoglycemia can cause seizures.

TIP: Chronic alcohol consumption causes total body depletion of magnesium stores, which in turn decreases the seizure threshold. The serum magnesium level may not accurately reflect the degree of depletion; a standard dose of 1 g magnesium is generally acceptable for a chronic alcoholic patient.

Neurological monitoring is also essential for the patient in alcohol withdrawal. Serial neurological checks will provide information on Mr. H.'s progress or deterioration with regard to the desired patient outcomes. The patient's orientation, general level of consciousness. degree and location of tremors, presence or absence of hallucinations. speech, and thought processes are all significant parameters to assess. Reorientation of the patient at frequent intervals should also be part of the nurse's interventions.

Before being discharged from the ED, Mr. H. should have achieved the desired outcomes as identified in the nursing plan of care. He and his family should be encouraged to seek assistance through follow-up care and to establish a regular care provider to restore his normal body functions. A detoxification referral is made, although Mr. H. has not given clear indications that he is ready for such a program.

REFERENCES

1. Mendelson JH In: Biochemical pharmacology of alcohol. Etron DH, et al.. eds. Psychopharmacology: a review of progress 1957-1967. PHS Publication #1836. U.S. Government Printing Office, Washington. D.C.. 1968.
   
   
2. Iber FL: In alcoholism, the liver sets the pace. Nutr Today 6:1:2-9, 1971.
   
   
3. Behnke RH: Recognition and management of alcohol withdrawal syndrome. Hosp Prac 11:79-84. 1976.
   
   
4. Victor M. Adams RD: The effect of alcohol on the nervous system. Research Publications - Association for Research in Nervous and Mental Disease 32:526-6:3.1953
   
   
5. Brown CG: The alcohol withdrawal syndrome. Ann Emerg Med 11:276-280, 1982.
   
   
6. Josephson GW, Sabatier HS: Rational management of alcohol withdrawal seizures. South Med J 71:1095-1097, 1978.
   
   
7. Victor M: A study of epilepsy in the alcoholic patient. In: Simmeon L, ed. Modern neurology. Boston: Little. Brown and Co.. 555-576. 1979.
   
   
8. Talbott GD. Gander 0: Convulsive seizures in the alcoholic: a clinical appraisal from the Baltimore Public Inebriate ate Program. Md St Med J 23:81-85,1974.
   
   
9. Victor M: Treatment of alcoholic intoxication and the withdrawal syndrome. Psychosom Med 28:636-650. 1966.

1.3 ALTERED MENTAL STATUS: TRICYCLIC ANTIDEPRESSANT DRUG OVERDOSE

Barbara Mlynczak-Callahan, RN, MS, CCRN

Rachel is a 26-year-old black female who is brought into the ED and is unresponsive to painful stimuli. The paramedics radioed ahead that the patient was found by her mother unconscious in her room. The patient's mother found an empty bottle of amitriptyline at Rachel's side. The amitriptyline was the mother's prescription that the mother had filled at the pharmacy the previous day. a supply of thirty 100-mg pills. On arrival to the ED the patient's BP is 90/40. pulse 144. respirations 6 and shallow. Her skin is warm and dry: her muscle tone is myoclonic. She is immediately taken to the resuscitation area for airway management, fluid resuscitation. and poisoning detoxification.

Triage Assessment. Acuity Level IV: Loss of consciousness, systolic BP < 90 mm Hg. pulse > 120 beats /min: respiratory rate < 12.

QUESTIONS AND ANSWERS

1. What is the immediate response of the ED nursing staff in the management of the patient with a drug overdose with loss of consciousness and significant cardiovascular instability?

   Rapid evaluations of the patient's airway, breathing, and circulation are the essential first activities in the management of the poisoned patient. For a patient such as Rachel who has a significant reduction in level of consciousness, protecting the patient's airway is critical. It is not unusual to move quickly to assist the physician to manually intubate and mechanically ventilate the patient.

   The patient's BP and heart rate are monitored closely for abnormalities. and volume expanders are given for significant hypotension. In virtually all cases of coma or altered mental status, the nurse should also anticipate the physician to order the following agents: glucose. 25 g to be administered intravenously over 3 to 4 min: naloxone (Narcan), 0.8 to 2 mg or 0.005 to 0.03 mg/kg intravenous push. repeated as many as 2 to 5 times (1). If alcoholism or malnutrition is suspected. 100 mg thiamine may be administered intravenously or intramuscularly. If the patient is experiencing seizures, intravenous diazepam or phenytoin may be indicated. Correction of acidosis. hypoxemia, electrolyte abnormalities, hypoglycemia, and hypo- or hyperthermia is essential to the survival of the patient (2, 3). In the case of tricyclic antidepressant (TCA) overdose, some consideration has been given to the use of physostigmine to counteract the anticholinergic effects of the drug. However, onset of seizure activity is a frequent occurrence when physostigmine is used, and, therefore, this treatment modality should be used with caution (4, 5).

   When the poison is unknown, additional assessments may be performed to determine the type of poisoning that has occurred. The assessment includes changes in vital signs, ocular signs, breath odors. skin signs, cardiopulmonary signs, and altered muscle tone (Table 1.3.1) (1, 2, 3). A 12-lead ECG should be obtained to assist with further differential diagnosis (Table 1.3.2) (1,2, 3). Routine blood samples obtained should include cell counts, electrolytes, glucose, ketones, liver and renal function indices, prothrombin time, arterial blood gases, and blood urine samples for toxicology screens. If the poison was ingested by mouth, a stomach wash is indicated for lab analysis of stomach contents. A chest x-ray is indicated to evaluate for pulmonary edema that could be caused by narcotics, barbiturates, salicylates, ethchlorvynol, or corrosive chemicals (1,2). Infiltrates may be present caused by aspiration of gastric contents or inhalation of metal fumes or hydrocarbons.

Table 1.3.1 Physical findings associated with various types of poisons