Medical Emergencies

CHAPTER 20 Medical Emergencies

Susan Engman Lazear, RN, MN , Anne Roberts, RN, BSN

General Strategy

Analysis: Differential Nursing Diagnoses/Collaborative Problems

Planning and Implementation/Interventions

Evaluation and Ongoing Monitoring

Documentation of Interventions and Patient Response

Age-Related Considerations

Specific Medical Emergencies

Reye’s Syndrome

Gout/Pseudogout

Allergic Reaction/Anaphylaxis

Chronic Fatigue Syndrome

Systemic Lupus Erythematosus

Rheumatoid Arthritis

I. GENERAL STRATEGY

A. Assessment

1. Primary and secondary assessment/resuscitation (see Chapter 1)

2. Focused survey

a. Subjective data collection

b. Objective data collection

1) General appearance

a) Level of consciousness, behavior, affect

g) Level of distress/discomfort

c) Rash or urticaria

d) Mucous membranes

e) Evidence of injury

f) Areas of erythema

g) Cardiac dysrhythmias on monitor

3) Auscultation

a) Breath sounds: clear, wheezes, crackles

b) Bowel sounds: normal, hyperactive, hypoactive, absent

c) Heart sounds: S₁ and S₂, other sounds (e.g., murmurs)

3. Diagnostic procedures

a. Laboratory studies

1) Complete blood count (CBC) with differential

2) Serum chemistries including glucose, blood urea nitrogen (BUN), and creatinine

3) Urinalysis; pregnancy test in female patients of childbearing age

4) Arterial blood gases (ABGs)

5) Erythrocyte sedimentation rate (ESR)

6) Serum and urine toxicology screen: therapeutic drug levels and toxic ingestion

7) Clotting profile: partial thromboplastin time (PTT), prothrombin time (PT)

8) Type and crossmatch

9) Serum ammonia level

10) Carboxyhemoglobin level

11) Serum uric acid level

12) Liver enzyme levels

13) Sickle cell screen

14) Hepatitis screen

15) Serum ketone levels

16) Thyroid function tests

17) Cerebrospinal fluid (CSF): cell count, glucose and protein count, culture

b. Imaging studies

1) Chest radiograph

2) Computed tomography (CT) scan

3) Magnetic resonance imaging (MRI)

1) 12- to 15-lead electrocardiogram (ECG)

2) Electroencephalogram (EEG)

3) Arthrocentesis

B. Analysis: Differential Nursing Diagnoses/Collaborative Problems

1. Ineffective airway clearance

2. Impaired gas exchange

3. Decreased cardiac output

4. Deficient/excess fluid volume

5. Ineffective tissue perfusion

6. Anxiety/fear

8. Impaired skin integrity

9. Deficient knowledge

10. Impaired memory

11. Ineffective coping

12. Acute/chronic pain

13. Risk for infection

14. Risk for injury

15. Disturbed sleep patterns

C. Planning and Implementation/Interventions

1. Determine priorities of care

a. Maintain airway, breathing, and circulation (seeChapter 1)

b. Provide supplemental oxygen as indicated

c. Establish intravenous (IV) access for administration of crystalloid fluid/medications as needed

d. Obtain and set up equipment and supplies

e. Prepare for/assist with medical procedures

f. Administer pharmacologic therapy as ordered

2. Relieve anxiety/apprehension

3. Allow significant others to remain with patient if supportive

4. Educate patient and significant others

D. Evaluation and Ongoing Monitoring (see Appendix B)

1. Continuously monitor and treat as indicated

2. Monitor patient’s responses/outcomes, and modify nursing care plan as appropriate

3. If positive patient outcomes are not demonstrated, reevaluate assessment and/or plan of care

E. Documentation of Interventions and Patient Response

F. Age-Related Considerations

1. Pediatric

a. Growth or development related

1) Dehydration occurs rapidly because of a smaller volume of fluid, large body surface area, and increased metabolic rate

2) Higher metabolic rate increases the use of glucose/glycogen stores

3) Neonates, infants, and toddlers are more susceptible to illness because of their immature immune system

b. “Pearls”

1) Lack of social smile is the single most significant indicator for a potentially ill child

2) Pediatric patients are unable to care for themselves during illness

3) Inspect neonates before touching them to diminish the startle response

4) Degree of fever does not reflect severity of illness

5) Administer medication dosages based on child’s weight

2. Geriatric

a. Aging related

1) Increased incidence of osteoporosis, osteoarthritis, joint cartilage atrophy, and gout

2) Immune system is compromised, leading to an increased risk of infection

3) Reserve capacity for responding to stress decreases

b. “Pearls”

1) Infections may manifest with a fall or generalized weakness, rather than with fever or elevated white blood cell (WBC) count

2) Subtle changes in orientation, appetite, or mood can indicate a medical problem

II. SPECIFIC MEDICAL EMERGENCIES

A. Reye’s Syndrome

Reye’s syndrome is an acute noninflammatory encephalopathy characterized by the triad of hepatic, metabolic, and neurologic dysfunction. Although the origin of Reye’s syndrome is unknown, the condition typically occurs in children following a viral illness such as influenza B, gastroenteritis, or varicella and is associated with the administration of aspirin during the illness. Parainfluenza, adenovirus, coxsackieviruses A and B, echovirus, Epstein-Barr virus (EBV), rubella, measles, cytomegalovirus, herpes simplex virus, parainfluenza viruses, and poliomyelitis viruses are less commonly involved than the other pathogens listed but can be the cause of Reye’s syndrome. The peak ages of developing Reye’s syndrome are 6 and 11 years. Six-year-old children are more likely to develop Reye’s syndrome following a varicella illness, whereas 11-year-old patients tend to develop the syndrome following influenza B illnesses. The greatest incidence occurs in late winter and early spring; more cases are reported in white patients living in rural or suburban areas.

The primary defect is mitochondrial injury. Glycogen stores are depleted as a result of starvation from prolonged vomiting and dysfunction of gluconeogenesis enzyme pathways. An alternative energy source is not available because fatty acid breakdown does not occur normally. Consequently, acids build up because the body cannot eliminate waste products effectively. The liver enzyme system that converts ammonia to urea is damaged, so ammonia also accumulates. Additionally, the liver and renal tubules become edematous and infiltrated with fat droplets. Fatty infiltrates develop in the heart, with petechiae throughout the epicardium. Hyperammonemia, hypoglycemia, and acidosis contribute to neurologic dysfunction, cerebral edema, and coma.

The manifestations of Reye’s syndrome are not unique to this syndrome. There is no test specific for Reye’s syndrome; therefore, the diagnosis must be one of exclusion. Signs and symptoms of Reye’s syndrome correlate with illness stages and include protracted vomiting with or without clinically significant dehydration, encephalopathy in afebrile patients with minimal or absent jaundice, and hepatomegaly in 50% of patients (Table 20-1). Some authorities postulate that antiemetics mask early symptoms, whereas others propose that antiemetics may further predispose the individual to the disease. Although it is rare, Reye’s syndrome needs to be considered in any child presenting with altered mental status and vomiting. An appropriate history should be obtained for all children presenting with symptoms similar to those of Reye’s syndrome to determine whether an inborn error of metabolism (IEM) should be considered. Diarrhea and hyperventilation may be the first signs in children younger than 2 years of age.

Table 20-1 STAGES OF REYE’S SYNDROME

Stage	Signs and Symptoms
Stage 0	Awake and alert
Stage I	Vomiting and lethargy or sleepiness Ability to obey commands Hepatic dysfunction EEG changes
Stage II	Delirium, combativeness, hyperreflexia, dilated pupils with sluggish response, tachycardia, appropriate response to noxious stimuli, hepatic dysfunction, EEG abnormalities
Stage III	Hyperventilation, obtunded, coma, decorticate posturing, normal pupillary and oculovestibular responses, continued hepatic changes, EEG changes
Stage IV	Deeper coma, decerebrate rigidity, fixed and dilated pupils, loss of oculocephalic reflex, abnormal oculovestibular reflex, minimal liver dysfunction, abnormal EEG findings
Stage V	Seizure, flaccidity, areflexia, dilated, nonreactive pupils, apnea, isoelectric EEG findings
Stage VI	Patients who cannot be classified because they have been treated with medication that alters level of consciousness

EEG, Electroencephalogram.

1. Assessment

a. Subjective data collection

b. Objective data collection

2) Diagnostic procedures

a) Serum ammonia level: elevated as much as 1.5 times normal (up to 1200 mcg/dL) 24 to 48 hours after the onset of changes in mental status and represents the most frequently seen laboratory abnormality; ammonia levels may return to the reference range in stage IV or V

(1) Less than 48 mg/dL (normal)

(2) Greater than 300 mg/dL (poor prognosis)

(3) Use heparinized blood tube on ice and send to laboratory

b) Liver enzyme levels: elevated

(1) Levels of transaminases, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) increase to three times normal but may return to the reference ranges by stage IV or V

c) Skeletal and cardiac isoenzymes: elevated

d) Coagulation profile: PT and PTT

e) Serum chemistries including glucose, BUN, and creatinine

(1) Glucose decreased; hypoglycemia present in children younger than 1 year of age because of their higher metabolism and lower glycogen stores

(2) Creatinine and BUN levels: mild to moderate elevation reflecting dehydration and acidosis

f) Amino and free fatty acid levels (e.g., glutamine, alanine, lysine): elevated

g) Factor assays: decreased factors II, VII, IX, and X and fibrinogen because of the disruption of synthetic activities in the liver

(1) Metabolic acidosis: increased anion gap

(2) Respiratory alkalosis

i) Serum bicarbonate: decreased secondary to vomiting

j) Lactate dehydrogenase (LDH): may be high or low

k) Bilirubin: greater than 2 mg/dL (usually less than 3 mg/dL) in 10 to 15% of patients; if direct bilirubin is more than 15% of total or if total is greater than 3 mg/dL, consider other diagnoses

l) Urine specific gravity: increased; 80% of patients have ketonuria

m) EEG: may reveal slow-wave activity in the early stages and flattened waves in advanced stages

n) CSF: opening pressure may or may not be increased; WBCs, usually lymphocytes, may be 9 × 10⁹/L (less than 9/mm³)

o) Head CT scan: may reveal cerebral edema, but results are usually normal

2. Analysis: differential nursing diagnoses/collaborative problems

a. Risk for ineffective airway clearance

b. Impaired gas exchange

c. Risk for deficient fluid volume

d. Ineffective tissue perfusion: cerebral

e. Ineffective family coping

3. Planning and implementation/interventions

a. Maintain airway, breathing, and circulation (seeChapter 1)

b. Provide supplemental oxygen as indicated

1) Rapid-sequence intubation (RSI) and ventilatory support in obtunded patients

2) High-flow oxygen

c. Establish IV access for administration of crystalloid fluids/medications as needed

1) Fluid challenge with 0.9% normal saline solution may be necessary

2) Avoid fluid overload in presence of cerebral edema: consider hypo-osmotic fluids

3) Colloid (e.g., albumin) solutions as necessary to maintain intravascular volume

d. Prepare for/assist with medical interventions

1) Advanced airway management

a) Nasal or oral intubation

b) Laryngeal mask airway

d) Surgical airway (e.g., cricothyrotomy)

2) Institute cardiac and pulse oximetry monitoring

3) Insert gastric tube and attach to suction

4) Insert indwelling urinary catheter

5) Catheter placement and monitoring of arterial pressure (see Chapter 7)

6) Catheter placement and monitoring of intracranial pressure (see Chapter 7)

7) Maintain normothermic or slightly hypothermic body temperature

8) Protect patient from injury (e.g., protective devices may be necessary if patient is combative, side rails up and locked)

9) Assist with hospital admission

10) Refer to National Reye’s Syndrome Foundation if diagnosis is confirmed

e. Administer pharmacologic therapy as ordered

1) RSI premedications: sedatives, analgesics, neuromuscular blocking agents

2) Dextrose to counteract hypoglycemia

a) If patient is initially hypoglycemic, administer dextrose 25% as an IV bolus at a dose of 1 to 2 mL/kg

b) If initial pH is less than 7.2, consider the administration of bicarbonate (somewhat controversial) up to 1 mEq/kg per hour; avoid rapid correction or overcorrection

3) Furosemide (Lasix) to control fluid overload

4) Insulin to maintain euglycemia

5) Sodium phenylacetate/sodium benzoate (Ammonul) for hyperammonemia; if the ammonia level is greater than 500 mcg/dL or if the patient’s condition fails to respond to the initial dose of sodium phenylacetate/sodium benzoate, start dialysis, preferably hemodialysis

6) Ondansetron (Zofran), 0.15 mg/kg (not to exceed 8 mg every 8 hours), during the first 15 minutes of initial dose of sodium phenylacetate/sodium benzoate: aids in offsetting GI effects of sodium phenylacetate/sodium benzoate

7) Phenytoin (Dilantin), 10 to 20 mg/kg IV for seizures as a loading dose, followed by 5 mg/kg IV per day in divided doses every 6 hours; or fosphenytoin (Cerebyx), dosed as 10 to 20 mg/kg phenytoin equivalents (PEs)

8) Osmotic diuretic: mannitol (Osmitrol)

10) Antipyretics (i.e., acetaminophen [Tylenol]); do not administer salicylates

4. Evaluation and ongoing monitoring (see Appendix B)

a. Airway patency

b. Level of consciousness

c. Hemodynamic status

d. Breath sounds and pulse oximetry

e. Cardiac rate and rhythm

f. Intake and output

g. Serum electrolyte levels

B. Gout/Pseudogout

Gout and pseudogout are the two most common crystal-induced arthropathies. They are debilitating illnesses in which pain and joint inflammation are caused by the formation of crystals within the joint space. Gout is inflammation caused by monosodium urate monohydrate (MSU) crystals and results from the overproduction or reduced secretion of uric acid. Thiazide diuretics and foods that are rich in purines increase the frequency of attacks. The first bout of gouty arthritis usually occurs at the first metatarsophalangeal joint. Pseudogout is inflammation caused by calcium pyrophosphate (CPP) crystals and is sometimes referred to as calcium pyrophosphate disease (CPPD). Many cases of pseudogout are idiopathic and are clinically indistinguishable from gout. Gout and pseudogout can be caused by lead poisoning, hemoproliferative disorders, and renal disease. Pseudogout has been associated with aging, trauma, and many different metabolic abnormalities, the most common of which are hyperparathyroidism and hemochromatosis. Gout has been associated with a large number of different autoimmune and metabolic disorders. Specific therapies and prophylactic measures have been developed to address the underlying problems. Treatment of the acute phase of pseudogout is identical to that of gout. Unlike gout, however, no specific therapeutic regimen exists to treat the underlying cause of pseudogout, and no known prophylactic therapy exists.

Three stages of gout occur: asymptomatic hyperuricemia, acute gout, and tophaceous gout. Nephrolithiasis may occur at any time. For gout, the male-to-female ratio is 9:1. Extra-articular deposits of MSU, known as tophi, may be seen along the Achilles tendon or on the ear helix, olecranon bursa, or prepatellar bursa. Acute monoarticular arthritis, septic arthritis, gout, and pseudogout can manifest in very similar ways (Table 20-2).

Table 20-2 COMPARISON OF GOUT, PSEUDOGOUT, MONOARTICULAR ARTHRITIS, AND SEPTIC ARTHRITIS

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Tags: Emergency Nursing Core Curriculum

Nov 8, 2016 | Posted by admin in NURSING | Comments Off

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