Complex special situations

Within 12 hours of this diagnosis, patient is becoming normovolemic evidenced by MAP at least 70 mm Hg, HR 60 to 100 beats/min (bpm), normal sinus rhythm on ECG, CVP 6 to 12 mm Hg, CI at least 2.5 L/min/m², bladder pressure measurements of less than 15 mm Hg, APP at least 60 mm Hg, stroke volume variation (SVV) less than 15%, urinary output at least 0.5 ml/kg/hr, warm extremities, brisk capillary refill (less than 2 seconds), and distal pulses at least 2+ on a 0 to 4+ scale. Although hemodynamic parameters are helpful to determine adequacy of resuscitation, serum lactate and base deficit are required to evaluate cellular perfusion.

Fluid Balance; Electrolyte and Acid-Base Balance

Fluid/electrolyte management

1. Monitor BP at least hourly, or more frequently in the presence of unstable vital signs. Be alert to changes in MAP of more than 10 mm Hg. Even a small but sudden decrease in BP signals the need to consult the physician or midlevel practitioner, especially with the trauma patient in whom the extent of injury is unknown.

2. Once stable, monitor BP at least hourly, or more frequently in the presence of any unstable vital signs. Be alert to changes in MAP of more than 10 mm Hg.

3. If massive fluid resuscitation was necessary for either the trauma patient or a patient with third-spaced fluid, the patient is at higher risk for IAH and should be observed closely for signs of decreased perfusion, respiratory distress, and deterioration in mental status.

4. In the patient with evidence of volume depletion or active blood loss, administer pressurized fluids rapidly through several large-caliber (16-gauge or larger) catheters. Use short, large-bore IV tubing (trauma tubing) to maximize flow rate. Avoid use of stopcocks, because they slow the infusion rate. Fluids should be warmed to prevent hypothermia.

5. Measure central pressures and CO continuously if possible, or at least every 2 hours if blood loss is ongoing. Calculate SVR and PVR if data is available at least every 8 hours—more often in unstable patients. Be alert to low or decreasing CVP and PAWP. Be aware that profound tachycardia (>120 bpm) will decrease the cardiac compliance and therefore normal pressure readings in this instance can be misleading. Also anticipate mild to moderate pulmonary hypertension, especially in patients with concurrent thoracic injury, such as pulmonary contusion, smoke inhalation, or early ARDS. ARDS is a concern in patients who have sustained major abdominal injury, inasmuch as there are many potential sources of infection and sepsis that make the development of ARDS more likely (see Acute Lung Injury and Acute Respiratory Distress Syndrome, p. 365).

6. Measure urinary output at least every 2 hours. Urine output less than 0.5 ml/kg/hr usually reflects inadequate intravascular volume in the patient with abdominal trauma. Decreasing urine output may also signify compression of the renal arteries in ACS.

7. Monitor for physical indicators of arterial hypovolemia, which may include cool extremities, capillary refill greater than 2 seconds, absent or decreased amplitude of distal pulses, elevated serum lactate, and base deficit.

8. Estimate ongoing blood loss. Measure all bloody drainage from tubes or catheters, noting drainage color (e.g., coffee grounds, burgundy, bright red). Note the frequency of dressing changes as a result of saturation with blood to estimate amount of blood loss by way of the wound site.

Electrolyte Management; Fluid Management; Fluid Monitoring; Hypovolemia Management

Ineffective tissue perfusion: gastrointestinal

Within 12 hours of this diagnosis, patient is becoming normovolemic evidenced by MAP at least 70 mm Hg, HR 60 to 100 beats/min (bpm), normal sinus rhythm on ECG, CVP 6 to 12 mm Hg, Bladder pressure measurements of less than 15 mm Hg, APP at least 60 mm Hg, CI at least 2.5 L/min/m², SVV less than 15%, urinary output at least 0.5 ml/kg/hr, warm extremities, brisk capillary refill (less than 2 seconds), and distal pulses at least 2+ on a 0 to 4+ scale. There should be a normal bicarbonate or total serum C0₂. By the time of hospital discharge, patient has adequate abdominal tissue perfusion as evidenced by normoactive bowel sounds; soft, nondistended abdomen; and return of bowel elimination.

Tissue Perfusion: Abdominal Organs

Circulatory care: arterial insufficiency

1. Identify patients who are at high risk for IAH.

2. Monitor BP at least hourly, or more frequently in the presence of unstable vital signs.

3. Monitor HR, ECG, and cardiovascular status every 15 minutes until vital signs are stable.

4. Auscultate for bowel sounds hourly during the acute phase of abdominal trauma and every 4 to 8 hours during the recovery phase. Report prolonged or sudden absence of bowel sounds during the postoperative period, because these signs may signal bowel ischemia or mesenteric infarction, which requires immediate surgical intervention.

5. Evaluate patient for peritoneal signs (see Box 3-3, p. 249), which may occur initially as a result of injury or may not develop until days or weeks later, if complications caused by slow bleeding or other mechanisms occur.

6. Ensure adequate intravascular volume.

7. Evaluate laboratory data for evidence of bleeding (e.g., serial Hct) or organ ischemia (e.g., AST, ALT, lactic dehydrogenase [LDH]). Desired values are as follows: Hct greater than 28% to 30%, AST 5 to 40 IU/L, ALT 5 to 35 IU/L, and LDH 90 to 200 U/L.

8. Measure bladder pressure manually: See Diagnostic Tests, Bladder Pressure Measurement, p 864.

9. Prepackaged closed system bladder pressure monitoring: Complete bladder pressure monitoring systems became available in approximately 2004. The system remains completely closed throughout the injection of fluid into the bladder, making it more desirable as part of prevention of catheter-associated urinary tract infections.

10. Assess for changes in level of consciousness, possibly resulting from increased IAP, which may inadvertently affect the draining of the cerebral veins.

Risk for infection

Patient is free of infection as evidenced by core or rectal temperature less than 37.7°C (100°F); normal white blood cell count and no bandemia; HR less than 100 bpm; orientation to time, place, and person; and absence of unusual redness, warmth, or drainage at surgical incisions and drain sites.

Immune Status; Infection Severity

Infection protection

1. Note color, character, and odor of all drainage. Report the presence of foul-smelling or abnormal drainage. See Table 3-2 for a description of the usual character of GI drainage.

2. As prescribed, administer pneumococcal vaccine to patients with total splenectomy to minimize the risk of postsplenectomy sepsis.

3. If evisceration occurs initially or develops later, do not reinsert tissue or organs. Place a saline-soaked gauze over the evisceration, and cover with a sterile towel until the evisceration can be evaluated by the surgeon.

4. For more interventions, see this diagnosis in Abdominal Trauma (p. 245).

Infection Control

Additional nursing diagnoses

Also see Major Trauma, p. 235. For additional information, see nursing diagnoses and interventions in the following sections: Hemodynamic Monitoring (p. 75), Prolonged Immobility (p. 149), Emotional and Spiritual Support of the Patient and Significant Others (p. 200), Peritonitis (p. 805), Enterocutaneous Fistula (p. 778), SIRS, Sepsis and MODS (p. 927), and Acid-Base Imbalances (p. 1).

Drug overdose

Overview/epidemiology

Drug overdose and accidental poisonings are common events, varying widely with respect to drug class, victim profile, and clinical scenario. Over 2 million human toxic exposure cases are reported to poison control centers annually. The 5 million total reported cases at all sites is probably an underestimation due to underreporting and misdiagnosing. Most cases are unintentional, involve a single agent, and can be handled on site with help from a poison control center; however, 5% to 10% of emergency department visits and 5% of ICU admissions involve exposure to toxic substances.

Type, amount, and route of use of the drug determine the effects, management, outcome, prognosis, and physical presentation. Every drug has a threshold for occurrence of serious toxic effects. Drugs of abuse are more dangerous than prescription drugs, as they are uncontrolled and unregulated, with a haphazard nature of administration. The patient’s history is often unavailable or of poor quality. Time is critical to successful treatment. A thoughtful and stepwise approach to laboratory testing, medical and nursing interventions, pharmacologic support, and general supportive measures is essential. No organ or body system is protected from the detrimental effects of drug overdose.

Ingestion of unknown substances

Many patients with drug overdose first arrive to be seen with altered mental status and without a useful or reliable history. Identification of the ingested substance is difficult. Lab screening is done for common drugs of abuse, including amphetamines, barbiturates, benzodiazepines, cocaine, opioids, phencyclidine, and cannabinoids. Specific drug levels are available for salicylates, acetaminophen, digoxin, theophylline, iron, and lithium. When one of these drugs is not the offending agent, a number of signs and symptoms should be noted and tests done to determine the list of potential offending agents.

Assessment

It is beyond the scope of this chapter to include all the drugs and toxins leading to common presenting symptoms, but important clues to the poison may be gleaned from answering the following questions:

• HR and rhythm: Is the patient bradycardic or tachycardic? Is a dysrhythmia present?

• Mental status: Is the patient overall depressed or agitated? Is delirium present?

• Temperature: Is hypothermia or hyperthermia present?

• Seizures: Is the patient having seizures?

• Eyes: Are pupils showing miosis or mydriasis? Is nystagmus present?

• Muscle tone: Is the patient flaccid or rigid? Are dyskinesias present?

• Lungs: If respiratory failure is occurring, is it related to depression, aspiration, edema, hemorrhage, bronchospasm, or cardiac failure?

• Arterial blood gas (ABG): Is the pH acidotic or alkalotic?

• Anion gap: If abnormal, is it increased or decreased?

• Blood glucose: Is the patient hyperglycemic or hypoglycemic?

• Psychosocial: Does the patient have a history of psychiatric disorders, of drug abuse, or of depression? Is the patient on any drugs with narrow therapeutic windows, and is a list of current medications (including over-the-counter [OTC]) available?

Diagnostic Tests for Drug Overdose

Drug	Diagnostic Lab Tests	Specific Considerations
Acetaminophen	Serum drug level	Therapeutic level: 10–20mcg/mL Draw level 4 hrs after ingestion. Subsequent levels are drawn according to the Rumack-Mathews nomogram until levels are below the predicted hepatotoxic range.
	Serum Na⁺, K⁺, CO₂, BUN, blood glucose, creatinine, liver enzymes, bilirubin; PT, coagulation studies; CBC; protein; amylase; ABGs
Alcohol Amphetamines Benzodiazepines Phencyclidine	Blood level; urine drug screen
Amphetamines Cyclic antidepressants	Serum K⁺, Na⁺, CO₂, BUN, glucose, creatinine, CBC, liver studies, cardiac enzyme levels with isoenzyme fractionations are monitored.
Barbiturates	Serum drug level
Barbiturates Benzodiazepines Cocaine Hallucinogens Opioids Phencyclidine Salicylates	Serum K⁺, Na⁺, CO₂, BUN, glucose, creatinine, CBC, ABGs, liver function studies
Cocaine	Urinalysis provides a quantitative method for identifying the presence of a cocaine metabolite.	Assessing blood levels of cocaine is usually of little diagnostic value.
Hallucinogens	Serum plasma drug level.
Opioids	Urine screening
Salicylates	Blood plasma level analyzed for presence of and amount	Repeat every 4 – 6 hours since the patient could have ingested sustained release drug
Cyclic Antidepressants	Blood plasma level; urine screen; gastric content analysis

Treatment options

Gastric decontamination is a general term referring to interventions used to prevent absorption of a toxin. Timely administration is essential for success. Best results are obtained if done within an hour of ingestion.

Activated charcoal

Activated charcoal is a fine, insoluble, nonabsorbable powder that binds with many toxic drugs to enhance their elimination. Activated charcoal does not bind with lithium, potassium, potassium chloride, ethanol, iron, acidic or alkaline corrosives, or hydrocarbons. Use is common and well researched and has proved efficacy in the preabsorption and postabsorption phases. The dose is 1 g/kg initially, followed by repeat doses of 0.5 to 1 g/kg every 2 to 4 hours. Combining the first dose with sorbitol increases the tolerability of charcoal, may help relieve constipation associated with charcoal, but has not been shown to enhance drug elimination. Contraindicated in cases of bowel obstruction or perforation and in patients with depressed mental status unless intubated.

Gastric lavage

Commonly known as “pumping the stomach,” insertion of nasogastric tube with vigorous enteral irrigation is a decreasingly important adjunct for treatment of ingested overdose; no longer recommended as routine management by the American and European toxicology associations. If used, it must be done as soon as possible and has little benefit if more than 60 minutes has passed since ingestion. When using lavage, the airway must be protected and lavage should continue until the fluid is clear of fragments (usually requires about 5 L of fluid). Gastric lavage should not be attempted if it delays or interferes with activated charcoal administration in appropriate patients.

Large, life-threatening amounts of ingested toxin (which may be poorly bound to activated charcoal used prior to lavage) may justify use. Additionally, patients at risk for esophageal hemorrhage or perforation should not be lavaged.

Whole bowel irrigation

The administration of a polyethylene glycol balanced electrolyte solution to rapidly cleanse the bowel may be useful in cases where activated charcoal is ineffective, such as with ingestions of iron, lithium, and sustained released tablets. It may diminish the effectiveness of activated charcoal, should not be done concurrently, and is contraindicated when ileus, GI bleeding, bowel obstruction, or bowel perforation is present.

Extracorporeal removal of toxins

Techniques include all types of dialysis, hemoperfusion, exchange blood transfusion and plasmapheresis. These methods are most often used to remove methanol, ethylene glycol, lithium, theophylline, salicylates, and phenobarbital. May be used in extreme cases when other management strategies are ineffective for drugs which are not highly protein bound, which have a reasonable molecular size, are water soluble (rather than lipid soluble), have a limited volume of distribution, and are not highly charged or ionized. Hemofilters used for continuous renal replacement therapy are often able to accommodate larger sized molecules than conventional hemodialysis therapy.

Commonly abused drugs

Acetaminophen (apap)

Acetaminophen is one of the most commonly ingested drugs in overdose. Most patients admit taking this drug. Unintentional overdose may happen due to polypharmacy, wherein APAP is contained in one or more other medications being used. Unintentional overdose is more common in children. Signs and symptoms of toxicity vary significantly depending on the dose, time elapsed since ingestion, and whether overdose resulted from acute or chronic ingestion. Toxicity from acute ingestion may be asymptomatic for up to 12 hours.

Oral (most common); rectal per suppository

Effects on body systems

Cardiovascular:

Hepatic damage may prompt cardiac complications including dysrhythmias, ischemia, and injury (chest pain/pressure, nausea, shortness of breath [SOB], T-wave inversion, and ST-segment elevation on ECG).

Respiratory:

Bronchospasm (wheezes and difficulty breathing) and tachypnea have been reported as a hypersensitivity reaction or as a side effect of N-acetylcysteine. See Collaborative Management section that follows.

Neurologic:

Coma and seizures

Hepatic:

Acute ingestion will cause hepatic necrosis, which can lead to liver failure. Hypoglycemia, right-sided abdominal pain, and nausea with vomiting may be noted, usually 1 to 2 days after ingestion.

Renal:

Acute tubular necrosis with renal failure is seen in some cases but often resolves.

Associated findings:

Hypophosphatemia, metabolic acidosis, hypothermia, thrombocytopenia, and hemorrhagic pancreatitis

Support of cardiovascular and respiratory systems:

Supplemental oxygen should be given if ABG values indicate a trend toward respiratory failure. If the patient has an ineffective or absent breathing effort, mechanical ventilation is provided. Serial ECGs monitor for dysrhythmias. Symptomatic ventricular dysrhythmias and bradyarrhythmias are treated per Advanced Cardiac Life Support (ACLS) guidelines.

Removing acetaminophen from the patient:

Intravenous N-acetylcysteine (Acetadote, Mucomyst-10, Mucosil-10, Mucosil-20) is the most current treatment, or a combination of activated charcoal and N-acetylcysteine (Mucomyst, NAC) can be administered orally or via a gastric tube. Activated charcoal effectively adsorbs APAP if given within 4 hours. Mucomyst prevents systemic toxicity; especially if given 8 to 10 hours after ingestion. Lavage is used only if less than 1 hour has elapsed since ingestion. Administration of the activated charcoal and NAC should not be delayed to perform lavage.

Treatment of nausea and vomiting:

Fluid replacement therapy with lactated Ringer solution or D₅NS; antiemetics, such as promethazine hydrochloride (Phenergan).

Rewarming:

A heating blanket is applied if patient has hypothermia.

Treatment of hypoglycemia:

Usually done with a bolus of D₅₀ and continuous infusion of D₅W, based on serum glucose results. Hypoglycemia occurs because of the potent hepatotoxic effects of acetaminophen.

Alcohol

Route of administration:

Oral

Support of cardiovascular and respiratory systems to prevent collapse:

Oxygen supplementation; treatment of ventricular dysrhythmias and bradyarrhythmias according to ACLS guidelines.

Fluid/potassium replacement:

Manage hypovolemia with IV fluid infusion. Include IV multivitamins (MVI) in fluid replacement, and provide thiamine IM to prevent Wernicke encephalopathy.

Removing alcohol from the patient:

As alcohol is metabolized, the blood alcohol level decreases 15 mg/dl/hr according to recent literature (legal limit for driving is less than 100 mg/dl). Coma may occur if the level is greater than 300 mg/dl, but this is influenced by each individual’s metabolic process and tolerance. When extreme amounts of alcohol have been absorbed into the system, the liver and kidneys may not be able to break down and excrete the alcohol. Hemodialysis may be used for a life-threatening intoxication.

Prevention of emesis:

Antiemetics are given, and a gastric tube is inserted and maintained at low continuous suction.

Anticipation and treatment of withdrawal:

Benzodiazepines are the drugs of choice for treating alcohol withdrawal. Lorazepam, which can be given IV, intramuscularly (IM), orally (PO), or sublingually (SL), is the preferred agent on most alcohol withdrawal protocols. Longer-acting agents (chlodiazepoxide and diazepam) are also used, because of the decreased risk of recurrent withdrawal and/or seizures. Oxazepam and lorazepam have a mechanism of metabolism that is less liver dependent and are useful in cases involving cirrhosis. Medications are given as needed for withdrawal symptoms. In patients at high risk for severe withdrawal symptoms, or if withdrawal would be dangerous, benzodiazepines may be given on a schedule. If withdrawal is severe and benzodiazepine doses become excessive, barbiturates may be added. Agents that have glutamate blocking properties, such as lamotrigine, memantine, and topiramate, are showing promise in alcohol detoxification.

Treatment of hypoglycemia:

A bolus of D₅₀ and continuous infusion of D₅W, based on serum glucose. Thiamine should be given before glucose to avoid sudden onset of heart failure and worsening neurologic impairment.

Treatment of delirium tremens (dts):

The most severe manifestation of withdrawal, which can result in death. Symptoms develop 48 to 96 hours after cessation of alcohol ingestion and include confusion, disorientation, delirium, agitation, severe diaphoresis, tachycardia, fever, and hypotension. DTs generally resolve within 3 to 5 days. Patients are sedated with benzodiazepines, allowed to rest and sleep, and oriented frequently to reality.

Treatment/prevention of seizures:

Alcohol withdrawal seizures may occur in a range from the first 6 to 48 hours to late onset at 10 days after abstinence. Benzodiazepines are given to raise the seizure threshold during the withdrawal period. Additional seizure management should reflect institution protocol. If the patient has a history of a primary seizure disorder, an anticonvulsant agent may also be indicated.

Prevention of wernicke-korsakoff syndrome:

Caused by thiamine deficiency and manifested by diplopia (the first real diagnostic clue), confusion, excitation, peripheral neuropathy, severe recent memory loss, impaired thought processes, and confabulation. Prophylactic administration of thiamine is recommended: IM thiamine on admission; supplemental oral thiamine; and multivitamins and multiminerals high in C, B complex, zinc, and magnesium. Multivitamins and minerals are given to prevent malnutrition related to inadequate food intake and malabsorption caused by alcohol’s irritating effect on the GI tract.

Ingestion of carbohydrates, either orally or parenterally, increases the body’s demand for thiamine. For patients with a history of chronic alcohol ingestion, administration of thiamine should precede administration of glucose to prevent sudden profound thiamine deficiency and irreversible neurologic impairment.

Amphetamines

Methamphetamine, speed, crystal meth, white crosses, ice, crank, ecstasy

Oral, IV, IM, intranasal, smoked

Support of cardiovascular and respiratory systems to prevent collapse:

Antidysrhythmic agents are given per ACLS guidelines to manage tachycardias. Ischemia is treated with nitrates; myocardial infarction is treated per ACLS guidelines for acute coronary syndromes.

Removing amphetamines from the patient:

For oral ingestion, activated charcoal is administered orally or via gastric tube. Acidification of the urine with ammonium chloride helps clear amphetamine.

Treatment of hypertension:

Antihypertensives such as nitroprusside (Nipride) or labetalol may be needed to decrease BP.

IV diazepam 0.1 to 0.2 mg/kg is administered slowly and repeated every 5 minutes until sedation is achieved. Lorazepam is an alternative benzodiazepine.

Psychosis:

Haldol 5 mg is given IM or IV. Repeat dose may be required to control behavior.

Treatment of hyperthermia:

A cooling blanket, antipyretics, and iced IV fluids are used.

Treatment of dehydration:

Done by fluid replacement, such as lactated Ringer solution and NS continuous IV infusions

Anticipation and treatment of rhabdomyolysis:

Usually treated with sodium bicarbonate infusion, mannitol, or furosemide (Lasix)

Barbiturates

See Table 11-2.

Table 11-2 COMMON BARBITURATES

Generic Name	Common Brand Name	Half-life (hr)
Amobarbital	Amytal	8–42
Secobarbital	Seconal	19–34
Pentobarbital	Nembutal	15–48
Phenobarbital	Luminal and others	24–140
Butabarbital	Butisol	34–42
Secobarbital/amobarbital	Tuinal	8–42

Note: Withdrawal symptoms can be correlated with the half-life of the drug that was used. Withdrawal from drugs with shorter half-lives produces more intense symptoms that last for shorter periods, whereas withdrawal from drugs with longer half-lives produces less intense symptoms that can be prolonged. Moreover, the severity of the withdrawal is directly related to the drug’s dosage.

Yellow jackets, reds, barbs

Oral, IV, IM

Support of cardiovascular and respiratory systems to prevent collapse:

Electrical rhythm is monitored; bradyarrhythmias are treated according to ACLS guidelines. After fluids are replaced, vasopressor therapy (see Appendix 6), including dopamine and norepinephrine bitartrate (Levophed), may be initiated for hypotension. Mechanical ventilation may be required, depending on the degree of hypoxia and CO₂ retention.

Removing barbiturates from the patient:

If less than 1 hour since ingestion, gastric lavage may be initiated (provided there is no delay in the administration of activated charcoal). Activated charcoal is administered orally or via gastric tube to bind with the substance in the stomach; hemodialysis may be used if patient is in stage 4 coma. Sufficient sodium bicarbonate should be given to alkalinize the urine to a pH of 7.5.

Phenytoin or diazepam may be given.

Sedation for withdrawal symptoms:

Typically the barbiturate that was ingested is tapered gradually to zero.

A gastric tube is inserted, which is then connected to low suction.

Treatment of nausea and vomiting:

Antiemetics are administered, usually IV promethazine hydrochloride.

Treatment of hypothermia:

A warming blanket is used.

Benzodiazepines

See Table 11-3.

Table 11-3 COMMON BENZODIAZEPINES

Generic Name	Common Brand Name	Half-life (hr)
Chlordiazepoxide	Librium and others	7–28
Diazepam	Valium and others	20–90
Lorazepam	Ativan	10–20
Oxazepam	Serax	3–21
Prazepam	Centrax	24–200*
Flurazepam	Dalmane	24–100*
Chlorazepate	Tranxene	30–100
Temazepam	Restoril	9.5–12.4
Clonazepam	Klonopin	18.5–50
Alprazolam	Xanax	12–15
Halazepam	Paxipam	14

^* Includes half-life of major metabolites.

Oral, IM, IV

Support of cardiovascular system to prevent collapse:

Electrical rhythm is monitored. Atrial fibrillation or flutter may be treated with digoxin or amiodarone, with initial rate control using diltiazem or beta-blockers. Severe supraventricular tachyarrhythmias may be treated with adenosine. Hypotension is treated with fluid replacement, followed by dopamine or norepinephrine (Levophed).

Support of respiratory system:

Apnea monitoring and mechanical ventilation may be indicated. Flumazenil administration may be considered if hypoventilation ensues. Naloxone may be added if mixed ingestion, including opiates, is suspected.

Removing benzodiazepines from the patient:

Gastric lavage is initiated if less than 60 minutes after ingestion; Activated charcoal is used to bind with the substance in the stomach.

Prevention of seizures:

Phenytoin is administered.

Gastric tube is inserted, which is then connected to low intermittent suction.

Identification of rhabdomyolysis:

Seizure activity and breakdown of muscle cause protein to precipitate in the kidneys, leading to renal failure. Increased BUN, creatinine, and urine protein values are noted. Prevention of seizures is the best treatment for prevention of rhabdomyolysis.

Treatment of hypothermia:

A warming blanket is used if indicated.

Flumazenil administration:

Sedative and respiratory depressant effects may be reversed by flumazenil (Romazicon). Repeat doses may be necessary, since the duration of action of many benzodiazepines exceeds that of flumazenil. Use with caution, especially in patients with possible multiple drug overdose. Flumazenil may precipitate seizures in benzodiazepine-dependent patients and causes arrhythmias in patients who also have high levels of cyclic antidepressants.

Cocaine

Crack, rock, freebase, snow

Nasal or IV (cocaine, snow); smoked (crack, rock, freebase)

Effects on body systems

Cardiovascular:

Hypertension; sinus tachycardia and sinus bradycardia; ventricular dysrhythmias such as premature ventricular contractions (PVCs), ventricular tachycardia, and ventricular fibrillation; myocardial infarction; heart failure; cardiomyopathy; acute endocarditis; and aortic dissection. Acute intoxication may result in profound hypotension and shock.

Respiratory:

Sharp pleuritic pain, hemoptysis, pneumothorax, bronchospasm, pulmonary edema, and respiratory failure. Both lactic acidosis and metabolic acidosis have been seen.

Neurologic:

The degree of CNS stimulation depends on the route and amount of drug taken. Headache, hyperexcitation, paranoia, delirium, hallucinations, tremors, and aggression may be seen. Mentation may vary from stimulated, euphoric, and excited states to delirium, stupor, and coma. Seizures are common, usually tonic-clonic, and may last for hours. Initially patients may seem well-coordinated, but later may show tremors and fasciculations as their condition deteriorates.

Renal:

Renal failure can occur and has been related to profound hypotension and rhabdomyolysis.

Associated findings:

Hyperthermia is common, and rectal temperatures may be elevated to as high as 43°C (109.4°F). Perforated nasal septum, track marks related to IV use, and mydriasis (dilated pupils) occur.

Indicators of withdrawal:

Poor concentration, anergia, anhedonia, bradykinesis, sleep disturbance, decreased libido, intense cocaine craving, depression, and suicidal tendencies

Indicators of cocaine psychosis:

Tactile and visual hallucination and paranoia

Peak action

• Intranasal—20 to 60 minutes

• Oral—60 to 90 minutes

• IV—5 minutes

• Smoked —less than 5 minutes

Cutting agents:

Cutting agents are substances mixed with pure cocaine to increase bulk. Cutting agents are often unknown but may include procaine, phencyclidine (“angel dust”), amphetamine, quinine, talc, and strychnine. Agents used in the preparation of crack include powdered cocaine, water, baking soda, and lidocaine. Cutting agents can become emboli that shower into cerebral and pulmonary circulation, with subsequent effects.

Collaborative management:

Support of cardiovascular system to prevent collapse: Electrical rhythm is monitored. Supraventricular tachycardia and ventricular dysrhythmias are managed according to ACLS guidelines. Monitor ECG for ischemic changes or infarction pattern (T-wave inversion or ST-segment elevation or depression).

Support of respiratory system:

Comatose patients are placed on mechanical ventilation.

Identification of route of administration and removing cocaine following oral ingestion:

A radiograph of the GI tract may reveal a cocaine-filled condom. Surgery may be performed to remove it. Activated charcoal may be administered to bind with cocaine in the stomach, or a laxative or suppository may be given to facilitate rectal excretion. An approach under investigation is to flush cocaine from the circulation using IV ammonium chloride.

Treatment of hypotension or hypertension:

Antihypertensives or vasopressors are administered as indicated.

Treatment of volume deficiency:

IV fluid replacement is done, such as with lactated Ringer solution or D₅NS.

Diazepam, phenytoin, or phenobarbital is administered.

Treatment of hyperthermia:

A cooling blanket, ice, and/or acetaminophen is used. Core temperature is the most accurate measurement.

A gastric tube is inserted, then connected to low continuous suction.

Cyclic antidepressants

Examples include amitriptyline hydrochloride (Elavil), doxepin hydrochloride (Sinequan), imipramine hydrochloride (Presamine, Tofranil), trimipramine maleate (Surmontil), nortriptyline (Pamelor, Aventyl), and desipramine (Norpramin).

Route of administration:

Oral

Collaborative management:

If the patient is symptom free, monitor for a minimum of 6 to 8 hours, noting vital signs and width of QRS complex.

Support of cardiovascular system to prevent collapse:

Electrical rhythm is monitored for at least 6 hours to enable assessment for a widening QRS complex, which is a signal of worsening toxicity. Supraventricular tachycardias are treated with adenosine or diltiazem; ventricular dysrhythmias are treated with antidysrhythmics such as amiodarone. Atropine and pacing may be indicated in the presence of symptomatic conduction defects.

Removing cyclic antidepressants from the patient:

Activated charcoal is administered via gastric tube to bind with the ingested substance in the stomach.

Reversal of the effects of the drugs:

IV sodium bicarbonate is used. An alternative approach is to promote a state of respiratory alkalosis by increasing respiratory rate via mechanical ventilation.

Phenytoin and diazepam are administered.

Respiratory support:

Mechanical ventilation is used. Pulmonary edema is treated with nitrates, morphine, diuretics, potassium replacement, and IPPB treatments.

Treatment of hypotension:

Fluid replacement is carried out, followed by administration of dopamine and norepinephrine (Levophed) as indicated.

Treatment of hyperthermia or hypothermia:

A cooling or a warming blanket is used as indicated.

A gastric tube is inserted, then connected to low intermittent suction.

Hallucinogens

Common agents:

Lysergic acid diethylamide (LSD), mescaline, morning glory seeds, nutmeg

Collaborative management:

Oral, IV, nasal, smoked

Support of cardiovascular system to prevent collapse: Manage BP and HR/rhythm according to ACLS guidelines.

Removing hallucinogens from patient:

If oral ingestion was within 1 hour gastric lavage may be attempted, as long as activated charcoal therapy is not delayed. Activated charcoal is administered orally or via gastric tube to bind with the substance in the stomach.

Prevention of seizures:

Anticonvulsants such as phenytoin or diazepam are administered.

Opioids

Examples of opioids include codeine, fentanyl, heroin, hydrocodone, hydromorphone hydrochloride (Dilaudid), levorphanol tartrate (Levo-Dromoran), meperidine hydrochloride (Demerol), methadone (Dolophine), morphine, opium, oxycodone hydrochloride (Percocet-5, Tylox, Oxycontin), and oxymorphone (Numorphan).

Oral, IV, IM, smoked

Support of cardiovascular system to prevent collapse:

Electrical rhythm is monitored; bradyarrhythmias are treated per ACLS guidelines. Vasopressor therapy is initiated for hypotension after fluids have been replaced.

Removal of orally ingested opioids from patient:

Activated charcoal is administered orally or via gastric tube to bind with the substance in the stomach.

Reversal of opioid effects:

Administration of naloxone hydrochloride (Narcan) to manage respiratory depression. After the initial dose of naloxone, the patient’s respiratory status must be monitored closely, since additional doses may be required. Respiratory depression and coma may occur when the effects of naloxone wear off and the opiate effects predominate. The half-life of naloxone is 60 to 90 minutes, and effects last 2 to 3 hours. If the narcotic effects last longer than the effects of the naloxone, the patient may slip into coma once the naloxone wears off. If persistent respiratory depression is present, a continuous naloxone infusion may be considered.

Treatment of drug withdrawal symptoms:

Hallucinations are treated with haloperidol (Haldol).

Support of respiratory system:

Pulmonary edema is treated with diuretics and restriction of IV fluid intake. An individual whose respiratory system is deteriorating is placed on apnea monitoring or mechanical ventilation.

A gastric tube is inserted, then connected to low continuous suction.

Prevention/treatment of seizure activity:

Anticonvulsant therapy is done, such as phenytoin administration.

Prevention of rhabdomyolysis:

See discussion in Benzodiazepines, p. 874.

Phencyclidine

PCP, angel dust, mist, peep, hog, crystal

Oral, nasal, smoked

Support of cardiovascular system to prevent collapse:

Electrical rhythm is monitored and tachydysrhythmias are treated as previously discussed. Nitroprusside is used for antihypertensive therapy. Nitroglycerin may be given to treat ischemia.

Removal of phencyclidine from the patient:

No specific antidote is available, although multiple administrations of charcoal to bind with the ingested substance in the stomach are standard practice. Charcoal is ineffective if phencyclidine was smoked, rather than swallowed. The first dose of charcoal may be accompanied with sorbitol. After ruling out the possibility of rhabdomyolysis, acidification of the urine with ammonium chloride or ascorbic acid to a pH around 5.5 is done.

Prevention/treatment of seizure activity:

Phenytoin and diazepam are given. Diazepam is administered IV at an initial dose of 2 to 5 mg. May be repeated every 30 minutes until sedation is achieved. Haldol may be given 5 to 10 mg IV to control psychosis. The effects of Haldol usually occur within 5 to 10 minutes of administration.

Respiratory support:

Pulmonary edema is treated with diuretics and restriction of IV fluid intake. Persons with hypoxia and respiratory distress require monitoring of pulse oximetry and may require mechanical ventilation.

A gastric tube is inserted, then connected to intermittent low suction.

Prevention of rhabdomyolysis:

See discussion in Benzodiazepines, p. 874.

Treatment of hypothermia or hyperthermia:

A warming or cooling blanket is used as appropriate.

Salicylates

Examples include aspirin, bismuth subsalicylate (Pepto-Bismol), and fendosal.

Oral, rectal (suppository)

Support of cardiovascular system to prevent collapse:

Electrical rhythm is monitored. Ventricular dysrhythmias and bradyarrhythmias are treated per ACLS guidelines.

Removal of salicylates from the patient:

Activated charcoal is administered orally or via gastric tube to bind with the substance in the stomach; several doses of activated charcoal may be necessary to achieve a 10:1 ratio of charcoal to salicylate. Hemodialysis may be necessary if the substance has been more extensively absorbed. Charcoal hemoperfusion may clear salicylates somewhat but cannot correct acid-base, electrolyte, and fluid problems associated with severe poisoning.

Fluid replacement:

Replace fluids with lactated Ringer solution or NS 20 ml/kg over 1 to 2 hours. Sodium bicarbonate may be added at a rate of 1 mEq/kg/hr to promote forced alkaline diuresis.

Potassium replacement:

See Fluid and Electrolyte Imbalances: Hypokalemia, p. 52.

Treatment of hyperthermia:

A cooling blanket or applications of ice is used.

Treatment of cerebral edema:

Hyperventilation (via mechanical ventilation) or mannitol is used.

Respiratory support:

Mechanical ventilation is used as indicated.

Treatment of pulmonary edema:

Nitrates, morphine, diuretics, potassium replacement, and intermittent positive pressure breathing (IPPB) are possible.

A gastric tube is inserted, then connected to low suction.

Replacement of blood loss:

Through delivery of blood and blood products

Specific antidotes for common drug overdoses/toxicities

Table 11-4 gives specific drug treatments for a few of the more common and critical drug overdoses not discussed in the preceding section.

Table 11-4 MANAGEMENT OF DRUG OVERDOSE/TOXICITIES

Target (toxic) Drug or Class	Treatment or Antidote
Acetaminophen	N-Acetylcysteine
Anticholinergics	Physostigmine
Arsenic, lead, mercury, or other heavy metals	Dimercaprol injection
Benzodiazepines	Flumezanil
Beta-blockers	Glucagon; beta agonists
Calcium channel blockers	Calcium IV, glucagon
Copper	Trientene
Cyanide	Sodium thiosulfate, sodium nitrite, amyl nitrite, hydroxocobalamin
Cyclic antidepressants	Sodium bicarbonate
Digitalis glycosides	Digoxin immune Fab
Heparin	Protamine
Insulin	Glucagon, dextrose, octreotide
Iron	Deferoxamine
Lead	Succimer, edetate calcium disodium (EDTA)
Methanol	Fomepizole, ethanol, folinic acid
Nitrites	Methylene blue
Opiates	Nalmefene, naltrexone, naloxone
Organophosphate insecticides	Atropine, pralidoxime
Warfarin	Vitamin K (IV or PO)

CARE PLANS FOR ALL DRUG OVERDOSES

Ineffective airway clearance

Chest radiograph normalizes. Within 2 to 24 hours of intervention/treatment, patient has a patent airway and is free of congestion as evidenced by clear breath sounds over the upper airways and lung fields, RR 12 to 20 breaths/min with normal depth and pattern, PaO₂ at least 90 mm Hg, PaCO₂ 35 to 45 mm Hg, pH 7.35 to 7.45, and SpO₂ at least 95%.

Respiratory Status: Airway Patency; Aspiration Prevention; Respiratory Status: Ventilation

Respiratory monitoring

1. Assess for respiratory distress hourly and as needed. Note secretions; stridor; gurgling; shallow, irregular, or labored respirations; use of accessory muscles of respiration; restlessness and confusion; and cyanosis (a late sign of respiratory distress).

2. Suction oropharynx, or use suction via endotracheal tube as needed.

3. Administer bronchodilators as appropriate.

4. Monitor ABG values for evidence of hypoxia (PaO₂ less than 90 mm Hg) and respiratory acidosis (PaCO₂ greater than 45 mm Hg, pH less than 7.35).

5. Monitor respiratory patterns; provide continuous apnea monitoring if available.

6. If patient has been placed on mechanical ventilation, monitor for indicators of airway obstruction (see Mechanical Ventilation, p. 99).

7. Monitor oxygen saturation continuously. Be alert to values less than 95% with response depending on patient’s baseline and clinical presentation.

8. Monitor for nausea and vomiting. Evaluate effects of antiemetics.

Airway Management, Aspiration Precautions

Hyperthermia

Optimally, within 24 to 72 hours of intervention, patient becomes normothermic.

Thermoregulation

With massive overdose, temperature regulation may never be achieved.

Temperature regulation

1. Monitor for hyperthermia: temperature greater than 38.3°C (greater than 101°F), pallor, absence of perspiration, and torso that is warm to the touch. If means are available, provide continuous monitoring of temperature. Otherwise, measure rectal, core, or tympanic temperature hourly and as needed.

2. Monitor effects of cooling blanket, cooling baths, and ice packs to the axillae and groin.

3. Maintain fluid replacement as prescribed. Monitor hydration status and trend of input and output (I&O).

4. Monitor neurologic status hourly and as needed until stabilized.

5. Monitor vital signs continuously or hourly and as needed until stabilized.

6. Administer and evaluate effects of antipyretic medications.

Fever Treatment; Vital Signs Monitoring; Medication Prescribing

Deficient fluid volume

Patient remains normovolemic as evidenced by urine output greater than 0.5 ml/kg/hr, moist mucous membranes; balanced I&O, BP within patient’s normal range, HR less than 100 bpm, stable weight, CVP 8 to 12 mm Hg, and PAWP 6 to 12 mm Hg.

Hydration; Fluid Balance

Fluid management

1. Monitor hydration status. Note signs of continuing dehydration: poor skin turgor, dry mucous membranes, thirst, weight loss greater than 0.5 kg/day, urine specific gravity greater than 1.020, weak pulse with tachycardia, and postural hypotension.

2. If the patient has a pulmonary artery catheter:

• Monitor SVR and pulmonary vascular resistance (PVR) as appropriate.

• Monitor CO as appropriate.

• Monitor PCWP/PAWP and central venous/right atrial pressures.

• Administer positive inotropic/contractility medications.

3. Evaluate the effects of fluid therapy.

4. Assess for indicators of electrolyte imbalance, especially the presence of hypokalemia. Be alert to irregular pulse, cardiac dysrhythmias, and serum potassium level less than 3.5 mEq/L.

5. Monitor I&O hourly; assess for output elevated disproportionately to intake, bearing in mind the insensible losses.

6. Monitor laboratory values, including serum electrolyte levels and serum and urine osmolality. Note BUN values elevated disproportionately to the serum creatinine (indicator of dehydration rather than renal disease), high urine specific gravity, low urine sodium, and rising Hct and serum protein concentration. Optimal values are the following: serum osmolality 275 to 300 mOsm/kg, urine osmolality 300 to 1090 mOsm/kg, BUN 10 to 20 mg/dl, serum creatinine 0.7 to 1.5 mg/dl, urine sodium 40 to 180 mEq/24 hr (diet dependent), Hct 37% to 47% (female) or 40% to 54% (male), and serum protein 6 to 8.3 g/dl.

7. Maintain fluid intake as prescribed; administer prescribed electrolyte supplements.

Fluid/Electrolyte Management; Surveillance; Hypovolemia Management

Disturbed sensory/perceptual perception: visual, tactile, auditory, kinesthetic,

Within 48 hours of intervention, patient verbalizes orientation to time, place, and ¬person and is free of abnormal sensory and perceptual experiences.

Cognitive Orientation; Distorted Thought Self-Control

Reality orientation

1. Establish and maintain a calm, quiet environment to minimize patient’s sensory overload.

2. Assess patient’s orientation to time, place, and person. Reorient as necessary.

3. Explain procedures before performing them. Include significant others in orientation process.

4. Do not leave patient alone if agitated or confused.

5. Administer antianxiety agents as prescribed.

6. If patient is hallucinating, intervene in the following ways:

• Be reassuring. Explain that hallucinations may be very real to patient but that they are not real, that they are caused by the substance that patient consumed, and that they will go away eventually.

• Try to involve family and significant others, because patient may have more trust in them.

• Explain that restraints are necessary to prevent harm to patient and others. Reassure patient that restraints will be used only as long as they are needed.

• Tell patient that you will check on him or her at frequent intervals (e.g., every 5 to 10 minutes) or that you will stay at patient’s side.

Delusion Management; Environmental Management; Fall Prevention; Surveillance: Safety

Risk for violence: self-directed and/or other-directed

Patient, staff, and patient’s significant others are free of injury.

Impulse Self-Control

Behavior management

1. If patient’s condition is stable, provide a sitter, or auxiliary staff member, such as an orderly or nursing assistant, to observe patient when awake.

2. Speak with patient in a quiet and calm voice, using short sentences.

3. Establish a therapeutic relationship with patient.

4. Encourage patient to take control over his or her own behavior.

5. Facilitate support by significant others.

6. Limit interventions.

7. Administer and evaluate effectiveness of sedation to calm patient.

8. Keep all sharp instruments out of patient’s room. Follow agency protocol accordingly.

9. Develop appropriate behavior expectations and consequences, given the patient’s level of cognitive functioning and capacity for self-control.

Behavior Management: Self-Harm; Substance Use Treatment: Alcohol Withdrawal; Substance Use Treatment: Overdose, Suicide Prevention

Additional nursing diagnoses

See nursing diagnoses and interventions in the following as appropriate: Nutritional Support (p. 117), Mechanical Ventilation (p. 99), Hemodynamic Monitoring (p. 75), Prolonged Immobility (p. 149), Emotional and Spiritual Support of the Patient and Significant Others (p. 200), Acute Lung Injury and Acute Respiratory Distress Syndrome (p. 365), Acute Respiratory Failure (p. 383), Acute Coronary Syndromes (p. 434), Heart Failure (p. 421), Cardiomyopathy (p. 482), Dysrhythmias and Conduction Disturbances (p. 492), Aortic Aneurysm/Dissection (p. 467), Acute Renal Failure (p. 584), Status Epilepticus (p. 668), Hepatic Failure (p. 785), Acute Pancreatitis (p. 762), Fluid and Electrolyte Disturbances, p. 37), and Acid-Base Imbalances (p. 1). In addition, see Traumatic Brain Injury for Impaired Corneal Tissue Integrity (p. 347).

High-risk obstetrics

Most pregnant women are healthy and rarely in need of critical care. Obstetric complications account for less than 1% of intensive care unit (ICU) admissions and less than 0.5% of all deliveries. Despite this relatively low incidence, the acuity of obstetric critical care patients is high due to the unique pathophysiology and clinical disorders associated with the pregnant patient. Maternal mortality rates range from 5% to 20% when pregnant women require critical care. Obstetric patients may be admitted into critical care due to complications of obstetric conditions, such as eclampsia, or complications of an underlying medical condition such as heart disease. Those with obstetric conditions are admitted more frequently and generally have better outcomes than those admitted with underlying medical conditions. Approximately 75% of obstetric critical care patients are admitted to the unit postpartum (after delivery). Obstetric hemorrhage and pregnancy-induced hypertension are responsible for approximately 50% of obstetric ICU admissions. This chapter will focus on the hypertensive complications of pregnancy that may result in admission to a critical care unit.

Caring for a pregnant patient presents the unique challenge of caring for the mother and the fetus simultaneously. Although survival of the mother will take precedence over fetal survival in most cases, the optimal outcome is survival of both the mother and fetus. Two basic principles should underlie the care of the pregnant patient. First, maternal anatomic and physiologic changes occur during pregnancy to facilitate adequate blood flow to the fetus and protect the mother after delivery (Box 11-2). The pregnant patient may require hemodynamic monitoring, and the critical care nurse should be familiar with the different hemodynamic changes and pressure values in pregnancy and labor as outlined in Table 11-5. Second, the fetus is totally dependent on the mother for all of his or her oxygenation and growth needs, so any intervention performed on the mother will most likely affect the fetus. Despite the unique challenges presented by the critically ill obstetric patient, transfer of the patient to a critical care unit should not be delayed.

Box 11-2 PHYSIOLOGIC ANATOMICAL CHANGES IN PREGNANCY

Body position

Supine hypotension: After 20 weeks, supine positioning significantly reduces CO and uterine blood flow by compressing the inferior vena cava.

Lateral positioning or hip wedge under right or left hip is recommended to displace the gravid uterus to avoid supine hypotension.

Cardiovascular

Heart rate: 10 to 15 bpm increase from prepregnancy rate by 32 weeks

Blood pressure: 10 to 15 mm Hg decrease from prepregnancy value between 14 and 24 weeks returning to prepregnancy value by 37 to 40 weeks’ gestation

Blood volume: 40% to 50% increase by 24 weeks

Stroke volume: 30% increase by 32 weeks

CO: 30% to 50% increase by 24 weeks

Fetal circulation

More than 10% of maternal CO is diverted into the uterine circulation. Maternal CO increases by at least 25% during pregnancy. Fetal oxygenation is dependent on maintenance of sufficient maternal CO.

Gastrointestinal

Gastric motility: Decreased

Gastric emptying time: Decreased

IAP: Increased

These changes can cause increased risk of aspiration with general anesthesia.

Neck/throat

Larynx: Displaced anteriorly; change prompts increased incidence of airway edema and bleeding, leading to failed intubation.

Pulmonary and acid-base balance

Oxygen consumption: Increases

Functional residual capacity and volume: Decreased by elevated maternal diaphragm, resulting in increased risk of rapid development of hypoxemia and apnea compared to the nonpregnant patient

Acid-base imbalance: Respiratory alkalosis

Renal

Glomerular filtration rate: Increased by 50% at term

Table 11-5 EXPECTED HEMODYNAMIC CHANGES DURING PREGNANCY, LABOR, DELIVERY, AND POSTPARTUM

Hypertensive disorders of pregnancy

Pathophysiology

Hypertensive disease occurs in up to 22% of pregnancies. Preeclampsia, eclampsia, and HELLP (Hemolysis, Elevated Liver enzymes, Low Platelets) are all part of a continuum of hypertensive disorders unique to pregnancy. The etiology of these diseases is probably related to early placental development. Risks to the baby include poor growth and prematurity. Risks to the mother include stroke, pulmonary edema, renal failure, liver rupture, and disseminated intravascular coagulation (DIC). The only definitive cure is delivery of the fetus and placenta. Signs and symptoms usually resolve within 24 to 48 hours after delivery. The overall goal of nursing care of the hypertensive pregnant patient is to avoid complications to the mother and deliver a healthy, mature neonate. (Refer to Box 11-3.)

Box 11-3 CLASSIFICATION OF HYPERTENSIVE STATES OF PREGNANCY

• Gestational: Mild hypertension that develops during pregnancy without additional PIH symptoms

• Preeclampsia: Hypertension that develops during pregnancy after 20 weeks’ gestation (except in molar pregnancies) with proteinuria

• HELLP syndrome: Severe form of preeclampsia with hemolysis, elevated liver enzymes, and low platelets, which may lead to DIC. Rarely patients may be normotensive with HELLP.

• Eclampsia: Preeclampsia complicated by seizures

• Chronic hypertension: Hypertension that is present prior to pregnancy or develops before 20 weeks’ gestation without a molar pregnancy

• Chronic hypertension with PIH: Preeclampsia and/or eclampsia superimposed on chronic hypertension

Preeclampsia

Preeclampsia is defined as hypertension or BP at least 140/90 mm Hg accompanied by proteinuria during the second half of pregnancy. Preeclampsia occurs in 5% to 8% of all pregnancies. Preeclampsia is more common in first pregnancies and in nonwhite women from low socioeconomic backgrounds. Eclampsia is defined as seizures or coma during pregnancy following preeclampsia. Overall, preeclampsia and eclampsia are responsible for 15% of maternal deaths, with most deaths due to complications resulting from eclampsia.

Preeclampsia is a systemic syndrome unique to pregnancy characterized by widespread arteriolar vasospasm resulting in increased peripheral vascular resistance. Areas of vasospasm cause breaks or roughened areas in the endothelial layer. These roughened areas trigger fibrin deposition and leakage of intravascular fluid into the extravascular space. Decreased colloid oncotic pressure contributes to fluid leakage and proteinuria. As preeclampsia worsens, blood flow through the rough vasospastic areas results in hemolysis and thrombocytopenia. The resulting end effect is decreased circulation and oxygenation to the maternal organ systems, the placenta and the fetus. The physiologic process of vasospasm manifests in the development of the classic symptoms associated with preeclampsia: hypertension, proteinuria, headache, blurred vision, scotoma, epigastric pain, decreased urinary output, and increased liver enzymes.

Risk factors for preeclampsia

Preeclampsia is more common in African American and Hispanic women and in women experiencing their first pregnancy at ages less than 18 years or older than 34 years. Additional risk factors for preeclampsia are pre-existing hypertension, diabetes, obesity, family history of preeclampsia, multifetal pregnancies, renal disease, connective tissue disease, and anti–phopholipid antibody syndrome.

Mild preeclampsia

Mild preeclampsia is characterized by BP at least 140/90, proteinuria (2 g in a 24-hour urine specimen), and creatinine greater than 1.2 mg/dl without accompanying maternal symptoms such as headache, vision changes, or epigastric pain. The treatment for mild preeclampsia is generally hospitalization with bedrest in a lateral position and close observation of maternal and fetal status. Mild preeclampsia can rapidly move from a mild disease state to the severe preeclampsia, eclampsia, or HELLP syndrome. The critical care nurse should observe the mild preeclamptic pregnant patient closely for signs that the disease process is worsening, such as headache, vision changes, altered lab values, epigastric pain, or deterioration in fetal status.

Signs of mild preeclampsia include:

• Hypertension: BP at least 140/90 mm Hg, on two separate occasions, at least six hours apart, during the last half of pregnancy

• Proteinuria: Increased to greater than 2 g in a 24-hour urine specimen

Severe preeclampsia

Severe preeclampsia suggests a worsening degree of vasospasm within the maternal and fetal circulation as evidenced by the presence of headache, blurred vision, scotoma, epigastric pain in the right upper quadrant, altered lab values and indications of fetal status deterioration. Goals of nursing management for severe preeclampsia include controlling maternal BP, avoiding eclampsia and facilitating fetal oxygenation and delivery.

Magnesium sulfate is the drug of choice for eclamptic seizures, although 10% of patients receiving magnesium therapy will develop subsequent seizures. Numerous studies have demonstrated that magnesium sulfate is superior to diazepam, lorazepam, phenytoin, and “lytic cocktail” in the management of eclampsia.

Signs of severe preeclampsia include:

• Hypertension: BP at least 160/110 mm Hg

• Proteinuria: Increased to greater than 5 g in a 24-hour urine specimen

• Interstitial Edema: Third-spaced fluids manifest as edema

• Serum creatinine: Increased to greater than 2 mg/dl

• Platelet count: Rapidly decreasing platelet count

• Oliguria: Decreased to less than 500 ml/24 hr

• Visual or cerebral disturbances: Blurred vision, altered thought processes

• Respiratory distress: Cyanosis or noncardiogenic pulmonary edema

• Intrauterine abnormalities: Fetal growth restriction and/or oligohydramnios (decreased amniotic fluid)

Refer to Table 11-6 for more specific changes in physiology.

Table 11-6 HEMODYNAMIC PROFILES IN OLIGURIC PATIENTS WITH PREECLAMPSIA

Eclampsia

The diagnosis of eclampsia is made when generalized seizures or coma develop in a preeclamptic woman. Less than 1% of preeclamptic women will become eclamptic. Eclampsia is responsible for most of the perinatal mortality attributed to the hypertensive disorders of pregnancy. The majority of eclampsia cases occur within the last 12 weeks of pregnancy. One fourth of eclampsia cases develop intrapartum, or during labor and delivery. Another one fourth of the cases develop postpartum, or following delivery, and may occur up to 6 weeks after delivery. Management of the eclamptic patient encompasses the same care goals as the severe preeclamptic with the addition of seizure management and any complications.

Although critical care nurses frequently manage grand mal seizures of nonobstetric etiology, management of eclamptic seizure requires an obstetric nurse and physician at the bedside to monitor fetal and labor status.

Hellp syndrome

Pathophysiology

HELLP syndrome is an acronym for a unique pregnancy condition representing the most severe diagnosis of the preeclampsia continuum. HELLP is an abbreviation for hemolysis, elevated liver enzymes, and low platelets. HELLP syndrome occurs in up to 10% of patients with severe preeclampsia. The etiology of HELLP is uncertain. Worsening of systemic arteriolar vasospasm produces liver damage, subcapsular hematoma, and DIC. DIC in pregnancy may also be caused by placental abruption (abruptio placentae), dead fetus syndrome, septic shock, transfusion reaction, and amniotic fluid embolism. Maternal complications from DIC include ARDS and acute renal failure. The HELLP patient should be closely monitored for right upper quadrant pain or shoulder pain because these complaints may be indicative of liver hematoma or liver rupture. Hemodynamic monitoring may be required to manage patients with HELLP syndrome.

Diagnostic Tests for Hellp Syndrome

Test	Findings
Complete blood count (CBC)	Hgb and Hct may be elevated (>35 Hct) and steadily rising with severe preeclampsia-eclampsia
Peripheral blood smear	Schistocytes or burr cells are present with HELLP syndrome
Urinalysis	Positive for protein spillage.
24 Hour urine collection	Mild/moderate: 0.3–5 g protein with normal urine output. Severe preeclampsia-eclampsia: >5 g protein with low urine output.
Serum albumin	Decreases as urine protein spillage increases. Severe: <2.5 mg/dl.
Liver enzymes	Aspartate transaminase (AST), alanine amino transferase (ALT), and lactate dehydrogenase (LDH) are elevated with severe preeclampsia-eclampsia and HELLP syndrome. Bilirubin may be elevated with HELLP.
Renal serum chemistry	Mild-moderate: BUN, creatinine, and uric acid levels may be elevated. Severe preeclampsia-eclampsia: BUN, creatinine, and uric acid will be elevated.
Platelet count	Mild-moderate: >100,000/mL. Severe preeclampsia-eclampsia and HELLP syndrome: <100,000/mL
Bleeding time	Prolonged when platelet count is <100,000/mm³.
Fibrinogen	Decreased (<300 mg/dl).
Screening coagulation tests (PT, PTT, thrombin time)	Normal unless the patient develops HELLP syndrome that progresses to DIC, wherein all values are elevated.

Collaborative care

Collaboration between the critical care and obstetrics nurses is necessary in providing safe and comprehensive obstetric critical care. Nurses from each specialty bring unique and complementary knowledge and skills for patient management. Obstetric nurses have experience with fetal heart monitoring and interpretation, and critical care nurses have experience with managing patients requiring invasive monitoring, ventilatory support, and specific critical care procedures. A written protocol should be established to facilitate maternal transfer from the obstetric unit to the ICU or to an institution that can provide the appropriate level of care for both the mother and the fetus before and after delivery, based on the situation at hand. The protocol should also include planning and support for both obstetric and critical care nurses to work collaboratively to care for the patient. If the baby has been delivered, families may desire unrestricted visitation, or the mother may desire to have the baby remain in her ICU room. The collaborative team should develop a plan of care to address the physiologic, psychosocial, and family needs of the patient.

Preterm complications: timing of delivery

Preeclampsia arising at 34 weeks’ (or more) gestation is generally managed by delivery. Fetal viability, or the gestational age at which the fetus can survive outside the womb, is generally thought to be 24–25 weeks’ gestation. After 34 weeks gestation, the majority of infants will avoid major complications from prematurity. Before 34 weeks, patients with severe preeclampsia-eclampsia require delivery unless the gestational age is less than 26 weeks, wherein attempts to prolong the pregnancy may be initiated. If the mother exhibits signs of HELLP syndrome, such as thrombocytopenia or epigastric or right upper quadrant pain, or has visual disturbances, delivery should be strongly considered regardless of fetal age, since the mother is at risk of life-threatening illness if delivery is delayed. Management of the severely preeclamptic patient will depend on three conditions: maternal status, fetal status, and gestational age. If the pregnancy is at least 34 weeks, delivery is planned as there is little benefit in prolonging gestation. If the pregnancy is 33 to 34 weeks, glucocorticoids are given to the mother to accelerate the development of fetal lung maturity. The glucocorticoids are given intramuscularly in two doses 12 hours apart with maximum effect achieved 24 hours after the second dose. Glucocorticoids are given to facilitate lung maturity. Both the maternal and fetal status must be closely monitored. If either deteriorates, definitive steps must be taken regarding plans for delivery. The medical team carefully and constantly weighs the benefits of delivery for the mother versus the risks of preterm delivery for the fetus. The decision to proceed to delivery in a preterm pregnancy should be made in consultation with the obstetrician, pediatrician, critical care physician, and neonatologist (if available).

The following are the factors to consider in choosing the best clinical placement for the patient based on availability of equipment, skills, and trained personnel:

• Is continuous electronic fetal monitoring available?

• Are there resources for the administration of and monitoring of medications for labor induction or augmentation, anesthesia, and analgesia?

• Are care providers appropriately trained to provide fetal resuscitation measures?

• Is timely access to operating rooms for emergency cesarean feasible?

• Are care providers able to provide maternal hemodynamic/cardiac/respiratory monitoring and treatment?

• Are there resources available for neonatal support should complications arise?

Preterm labor

Most obstetric complications increase the risk of preterm labor, which is defined as labor that occurs prior to 37 weeks’ estimated gestational age (EGA). Most infants between 35 and 37 weeks’ gestation will transition to extrauterine circulation without difficulty. Signs and symptoms of preterm labor may be subtle and are likely to go unnoticed by nurses unfamiliar with labor assessment.

2. If patient has any signs or symptoms of labor, notify the physician or midlevel practitioner and:

• Position mother in the lateral position (turn to the left or right side).

• Encourage bladder emptying every 2 hours.

• Report all new onset of contractions or any change in contraction pattern immediately to the obstetrician or midlevel practitioner, because cervical examination is the most accurate method for diagnosing preterm labor.

3. Monitor uterine contractions (preterm labor) and fetal status:

• Preterm labor contractions may be infrequent, irregular, and painless or frequent, regular, and painful. Preterm labor, left undetected and untreated, can progress into an emergency delivery of a neonate within the critical care unit.

• Tocolytics or medications are used to stop preterm labor, but they must be started early in the labor process to be effective.

If frequent strong, painful uterine contractions continue, notify the obstetrician immediately as placental abruption may be occurring. Placental abruption refers to the detachment of the placenta from the wall of the uterus, which will result in life-threatening maternal hemorrhage. The only definitive treatment of a complete placental abruption is delivery of the fetus by cesarean section within minutes.

4. Provide fetal surveillance:

Fetal viability, or the gestational age at which the fetus can survive outside the womb, is generally thought to be 24 weeks’ gestation. An electronic fetal monitor has two external devices, which are strapped to the maternal abdomen, and includes a transducer that records fetal HR and a tocodynamometer, or “toco,” that records uterine activity. A continuous paper tracing can be produced for documentation. Volume control can be used to produce sound with each heartbeat or decreased to minimize noise, although most mothers enjoy hearing their baby’s heartbeat and may become worried if the sound is muted.

• On admission: Ultrasound, Doppler flow studies, biophysical profile, and amniotic fluid volume studies are ordered to evaluate fetal well-being. Between 14 to 24 weeks’ gestation, the fetal heart rate (FHR) is generally evaluated with a Doppler or fetoscope. Note the absence of FHR by Doppler does not confirm fetal death.

• Initiating electronic fetal monitoring: Monitoring of the FHR with an electronic fetal monitor typically is not begun until viability has been established. The timing of the initiation of electronic fetal monitoring will vary according to institutional protocol, medical provider, and/or patient situation.

The use of an electronic fetal monitor requires an obstetric registered nurse with appropriate training and competency in fetal heart rate interpretation. This can be achieved by the requirement of having both a critical care and an obstetrics nurse at the patient’s bedside. Having a labor nurse “on-call” if the critical care nurse notices an abnormal fetal heart rate or the onset of labor is not sufficient and compromises patient safety.

• Fetal nonstress testing: A Non-Stress Test (NST) is a frequently ordered non-invasive test to monitor fetal status. NSTs are performed by the obstetric nurse who is trained in the procedure and interpretation of NST results. This test is used to determine fetal well-being and is reflective of fetal oxygenation and placental function. It is often ordered daily on patients who are stable and not in labor. The NST is an assessment of continuous FHR and uterine activity over a 20- to 30-minute period using an electronic fetal monitor. Test results are interpreted as reactive, nonreactive, equivocal, or unsatisfactory, based on the presence or absence of FHR accelerations or decelerations over a 20-minute period. A reactive NST indicates adequate fetal well-being. A nonreactive NST may indicate a problem with placental functioning or fetal oxygenation and should be followed up with additional testing.

• Biophysical Profile: The Biophysical Profile (BPP) uses a combination of NST and fetal parameters observed via ultrasound to measure fetal well-being. The fetus is scored either 0, 1, or 2 for each of five parameters: fetal breathing movement, gross fetal movement, fetal tone amniotic fluid volume, and NST test results. BPP results of 8–10 indicate a normal fetus (when amniotic fluid volume is adequate). BPP results of 4–5 are considered equivocal and BPP results of < 4 indicate are considered abnormal.

• Amniocentesis: Withdrawal of amniotic fluid under direct ultrasonograpy is called amniocentesis. Examination of amniotic fluid can be used to determine fetal maturity in pregnancies < 34 weeks. An LS (lecithin: sphingomyelin) ratio of > 2:1 represents fetal maturity.

Positioning of the pregnant patient

The supine position should be not be used with pregnant women after 20 weeks’ EGA. At that time, the maternal vena cava is compressed by the growing maternal abdomen when the mother lies in a supine position. This effect is called “supine hypotension” and, if left unchecked, will lead to decreased blood return to the heart, decreased maternal BP, decreased CO, and subsequently to decreased blood flow to the uterus, placenta, and fetus. The appropriate position for the pregnancy patient is lateral positioning, which avoids the risk of supine hypotension and maximizes blood flow to the uterus, placenta, and fetus. Turning some pregnant women on the left side may improve CO more than the right side. Semi-Fowler’s positioning with a hip roll tilting the maternal abdomen off of the vena cava is another acceptable position for the pregnant woman in the latter half of pregnancy.

Blood pressure control and management

Control of maternal BP is essential to the care of the preeclamptic patient. The goal of therapy is to maintain BP less than 160 mm Hg systolic and less than 110 mm Hg diastolic. Sudden or extreme drops in maternal BP should be avoided as they may precipitate maternal stroke and/or decreased blood flow to the fetus. Venodilators are often used to lower BP. In pregnancy, the effect of the drug on the fetus must be considered. Antihypertensive agents used in pregnancy are chosen because of their ability to avoid vasodilation of placental vessels. The most commonly used antihypertensives are:

• Hydralazine 5 to 10 mg may be given every 10 to 15 minutes. Maximum dosage: 30 mg

• Labetalol 20 to 40 mg may be given every 10 to 15 minutes. Maximum dosage: 220 mg

• Labetalol should be used cautiously in patients with asthma and cardiac failure.

• Nifedipine 10 to 20 mg may be given every 30 minutes. Maximum dosage: 50 mg

Fluid management

Severely preeclamptic patients are easily overloaded with IV fluid predisposing them to pulmonary edema. Strict observation of intake and output is warranted. Total fluid intake is typically maintained at 125 to 150 ml/hr. Hemodynamic monitoring may be indicated if pulmonary edema develops. Urine output of less than 100 ml/4 hr should be reported to the physician or midlevel practitioner.

A nonglucose solution should always be available as part of a fetal resuscitation protocol, and a bolus of 500 to 1000 ml of lactated Ringer or normal saline is usually given to improve maternal circulating volume and subsequently improve uterine perfusion and fetal oxygenation.

Pain management

Generally speaking, medications used in pregnancy should be limited to Classes A and B whenever possible, to decrease potential negative effects on the fetus. The benefits of medications in Classes C, D, and E should be carefully weighed against the risk to the fetus. Butorphanol (Stadol), Nalbuphine (Nubain), and Fentanyl (Sublimaze) may all be given IM or as an IV bolus/IV push and are commonly given for pain relief during labor.

Meperidine (Demerol) and morphine are not often used due to their long half-life and potential to cause neonatal neurobehavioral depression, which may last several days.

Neuraxial analgesia techniques (spinal, epidural, or combined spinal-epidural) are commonly used because they are more effective at relieving pain and do not cause respiratory depression in the mother or fetus. Medications used are generally a combination of local anesthetics and opioids, which produce greater pain relief with less motor block than local anesthetics alone. Lumbar epidurals may be given continuously or as a patient-controlled analgesia (PCA). Contraindications to neuraxial analgesia include allergy to local anesthetics, when the last dose of low-molecular-weight heparin has been within 12 hours, coagulation disorders, maternal shock, or infection at the insertion site. Common side effects of neuraxial analgesia include maternal hypotension and itching. Hypotension is generally treated with IV fluid boluses and/or IV Ephedrine. Ephedrine is the preferred vasopressor because it causes peripheral vasoconstriction without affecting the umbilical vessels. Loratadine (Claritin) or Cetirizine (Zyrtec) may be given to alleviate itching.

Prevention of eclampsia/seizure management

Magnesium sulfate is the most effective anticonvulsant for preeclampsia, eclampsia, and HELLP syndrome, reflected by the Magpie Trial International Study Collaborative.

Magnesium sulfate is listed as a high-risk medication by The Joint Commission (formerly the Joint Commission on Accreditation of Healthcare Organizations [JCAHO], 2003). Obstetric nurses should be familiar with safety recommendations related to the administration of magnesium sulfate to pregnant or delivered patients.

Magnesium is given IV as a loading (bolus) dose followed by a continuous drip. Magnesium works by decreasing the maternal seizure threshold and relaxes the uterine smooth musculature by decreasing or stopping uterine contractions. The patient receiving magnesium is at higher risk for postpartum hemorrhage due to uterine atony (failure of the uterus to contract after delivery). Magnesium is metabolized by the kidneys so a decrease in urine output will cause a subsequent rise in magnesium levels.

Administration of magnesium sulfate:

• Administer using an infusion pump. Two nurses should verify the infusion pump settings when magnesium is initiated or dosage changed.

• Magnesium solutions should be premixed and labeled in standard solutions.

• An initial loading dose of 4 to 6 g is given over 15 to 30 minutes followed by a maintenance dose of 2 to 3 g/hr.

• Magnesium therapy is continued after delivery for 12 to 24 hours. Side effects of magnesium include flushing, nausea, muscle weakness, headache, and toxicity.

• Magnesium levels greater than 8 mg/dl are associated with signs of toxicity; refer to Table 11-7.

• If toxicity is suspected: Discontinue infusion, administer oxygen, obtain stat magnesium level, and notify physician.

• The antidote for magnesium toxicity is calcium gluconate 10 mg of 10% calcium gluconate solution IVP over 10 minutes and should be readily available.

• Serum magnesium levels are drawn 2 hours following the loading dose, then every 6 hours.

• Continuously use electronic fetal monitoring.

Table 11-7 CLINICAL EFFECTS OF MAGNESIUM

Serum Magnesium Level	Signs/Symptoms to Watch for
1.7–2.4 mg/dL	Normal
5–8 mg/dL	Therapeutic
8–12 mg/dL	Loss of pateller reflexes
10–12 mg/dL	Somnolence
12–16 mg/dL	Respiratory difficulty and depression
15–17 mg/dL	Muscle paralysis
>18 mg/dL	Altered cardiac conduction
30–35 mg/dL	Cardiac arrest

The patient must be closely monitored during magnesium administration. It is recommended that the obstetric nurse be present at the bedside with the critical care nurse to monitor fetal and uterine response during magnesium therapy. The desired therapeutic level of magnesium is 5 to 8 mg/dl. If magnesium toxicity is suspected, discontinue the magnesium infusion, support oxygenation and notify the physician immediately (Simpson, 2004).

Preparation for delivery

Labor and delivery of the critically ill obstetric patient may occur either in the labor and delivery unit or the critical care unit, depending on several factors. A multidisciplinary discussion by medical specialists and nursing regarding the pros and cons of critical care versus the use of the delivery room or operating room setting will determine the best placement of the patient for optimal maternal and fetal care during labor and delivery.

Vaginal delivery is the safest method of delivery for the HELLP patient with a cervix that is favorable for induction of labor. Cesarean should be reserved for obstetric indications. The goal of delivery method is to minimize the incidence of complications. If operative delivery is the selected method of delivery, 5 to 10 units of platelets may be ordered preoperatively for a platelet count of less than 50,000 mm³. The patient should be typed and cross-matched for blood and blood products to be used if hemorrhage and/or DIC develops intraoperatively or postoperatively. General anesthesia is typically selected, since regional anesthesia (entering the spine) is generally contraindicated with thrombocytopenia. Due to the potential for difficult intubation due to airway edema and hyperemia, fiberoptic intubation may be used. The patient will require close observation postoperatively for the first 24 to 48 hours.

Emergency delivery in the critical care unit

To improve communication and facilitate timely emergency response, the names, specialty, and pager/cell phone numbers of the medical and nursing care team members should be compiled on one sheet of paper or written on one specific white board in all of the units possibly involved in the care of the pregnant critical care patient. The teams would minimally include the medical and nursing personnel from critical care, labor and delivery, anesthesiology, neonatology, and possibly the nursery and respiratory therapists. Other medical specialists should be added as appropriate for the patient’s condition. It is helpful to have core team members communicate every shift to discuss emergency plans and update the plan of care and discuss any possibility of emergent interventions.

CARE PLANS FOR THE HIGH-RISK OBSTETRIC PATIENT IN CRITICAL CARE

Ineffective protection

Within 1 hour of development of severe preeclampsia, eclampsia, or severe HELLP syndrome, the pregnant patient (mother and child) is monitored intensively and prepared for delivery, to avoid life-threatening complications of pregnancy-induced hypertension.

Blood Coagulation; Fetal Status: Intrapartum

Electronic fetal monitoring: intrapartum

1. Verify HRs of mother and fetus prior to initiating electronic monitoring.

2. Monitor BP of mother at least every 5 minutes if severe hypertension or seizures have occurred. Monitor FHR for slowing, indicative of fetal distress.

3. Initiate fetal resuscitation measures to treat abnormal fetal heart rhythms, as appropriate. Note response to all supportive interventions.

4. Instruct woman and support person(s) about the need for monitoring and data to be obtained.

5. Keep physician informed of significant changes in FHR, interventions for abnormal patterns, fetal response, labor progress, and maternal response to interventions.

6. Administer anticonvulsive medications as ordered to control seizures.

7. Monitor magnesium levels, and be alert to hypermagnesemia: decreased respiratory rate and depth, loss of deep tendon reflexes.

8. Assist with application of forceps or vacuum extractor, as needed, during delivery.

9. Monitor the patient closely for hemorrhage if HELLP syndrome is present.

10. Note Hgb and Hct levels before and after blood loss, as indicated.

11. Monitor coagulation studies, including prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen, fibrin degradation products (FDPs), fibrin split products (FSPs), and platelet counts as appropriate.

High-Risk Pregnancy Care; Surveillance: Late Pregnancy

Ineffective protection

Throughout the hospitalization, patient remains free of seizures and neurologic complications as evidenced by orientation to time, place, and person; normoreactive pupils and reflexes; patient’s normal visual acuity, motor strength, and coordination; and absence of headache and other clinical indicators of increased intracranial pressure (IICP).

Fetal Status: Antepartum; Blood Coagulation; Fluid/Electrolyte Management

Seizure precautions

1. Monitor for and document seizures. Protect patient from injury by initiating seizure precautions. When patient is seizing, turn her to the side to promote placental perfusion and prevent aspiration.

2. Assess patient for initial signs of increased ICP, including diminished LOC, headaches, abnormal pupillary responses (i.e., unequal; sluggish/absent response to light), visual disturbances, weakness and paralysis, slow HR, and change in respiratory rate (RR) and pattern. Patient may be experiencing problems related to seizure management, or may experience intracranial bleeding if platelets are extremely low.

3. Monitor trend of Glasgow Coma Scale if patient has difficulty awakening after seizures. If patient exhibits signs of magnesium toxicity, consult physician and consider calcium gluconate administration.

4. Increase frequency of neurologic monitoring as appropriate.

5. Assess the epidural site (as appropriate), if patient received epidural analgesia during labor and delivery. Patients with coagulopathy may develop an epidural hematoma, manifested by sensory or motor deficits, bowel or bladder dysfunction, or back pain. Report problems to the physician immediately. The epidural catheter should remain in place until coagulation studies normalize.

6. Avoid activities that increase ICP.

7. If initial signs of IICP are noted, consult physician immediately. Signs of impending herniation include unconsciousness, failure to respond to deeply painful stimuli, decorticate or decerebrate posturing, Cushing triad (i.e., bradycardia, increased systolic BP, widening pulse pressure), nonreactive/fixed pupils, unequal pupils, or fixed and dilated pupils. See Traumatic Brain Injury, p. 333, for more information about herniation. For additional interventions for IICP, see Box 3-7.

Cerebral Perfusion Promotion; Neurologic Monitoring; Seizure Management

Risk for deficient fluid volume

Patient remains normovolemic as evidenced by HR, RR, and BP within 10% of expected normal range; urinary output 0.5 ml/kg/hr or greater and absence of epigastric or abdominal pain or tenderness, and frank bleeding resulting from HELLP syndrome.

Fluid Balance

Fluid monitoring

1. Monitor fluid status, including I&O, signs of hypovolemia, including increases in HR and RR, decreases in BP and urinary output, restlessness, and vital signs.

2. Initiate hemodynamic monitoring if necessary to assess shock state and/or manage hemodynamics.

3. Monitor Hgb and Hct as ordered. Postpartum, the uterus contracts and blood is released into the central circulation as it decreases in size. With a normal 500-ml vaginal delivery blood loss, often the Hgb and Hct increase despite the blood loss.

4. Inspect for bleeding from mucous membranes, bruising after minimal trauma, oozing from puncture sites, and presence of petechiae. Maintain patent IV access.

5. Administer supplemental oxygen as necessary for active bleeding.

6. Perform fundus checks and initiate gentle fundal massage to help the uterus remain firm and promote hemostasis.

7. Initiate bleeding control therapy as ordered. Methylergonovine, ergonovine, and carboprost may be used to manage prolonged bleeding or hemorrhage.

8. Replace lost volume with plasma expanders (e.g., albumin, hetastarch) and/or blood products as indicated. See Table 10-3 for information about blood products.

Fluid Management; Fluid/Electrolyte Management; Surveillance: Late Pregnancy; Bleeding Reduction; Hypovolemia Management

Risk for infection

Patient is free of infection as evidenced by normothermia, HR less than 100 bpm, RR less than 20 breaths/min, negative culture results, WBC count less than 11,000/mm³, clear urine, and clear, thin sputum.

Immune Status; Infection Severity

Infection protection

1. Monitor vital signs for evidence of infection (e.g., increases in heart and respiratory rates). Check rectal or core temperature every 4 hours for increases.

2. If temperature elevation is sudden, obtain specimens for blood, sputum, and urine cultures or from other sites as prescribed. Consult physician or midlevel practitioner for positive culture results.

3. Monitor CBC, and consult physician for significant increases in WBCs. Be aware that a normal or mildly elevated leukocyte count may signify infection in patients with liver dysfunction.

4. Evaluate secretions and drainage for evidence of infection (e.g., sputum changes, cloudy urine).

5. Evaluate IV, central line, and other site(s) for evidence of infection (i.e., erythema, warmth, unusual drainage).

6. Provide routine episiotomy care by spraying the area with warm water at least every 4 hours. Sitz baths are usually not possible with critically ill patients. Ice packs and topical anesthetics may be used to enhance comfort.

7. Provide daily breast care by cleansing the breasts with mild soap and water. Breast engorgement should be managed per physician’s orders to help prevent infection and control pain. If left unrelieved, breast engorgement can result in stoppage of lactation. If breast-feeding is planned, breasts can be massaged and milk manually expressed or pumped.

8. Prevent transmission of infectious agents by washing hands well before and after caring for patient and by wearing gloves when contact with blood or other body substances is possible. Dispose of all needles and other sharp instruments in puncture-resistant, rigid containers. Keep containers in each patient room and in other convenient locations. Avoid recapping and manipulating needles before disposal. Teach significant others and visitors proper hand-washing technique. Restrict visitors with evidence of communicable disease.

9. Administer antibiotics as prescribed. Use caution and reduced dosage when administering antibiotics (especially aminoglycosides) to patients with low urinary output or renal insufficiency.

Compromised family coping

Patient and family demonstrate adequate coping behaviors and are facilitated in being together as soon as possible in the postpartal hospitalization.

Family Coping; Family Normalization

Coping enhancement

1. Provide regular updates to family members about the condition of both mother and infant.

2. Invite family members to participate in care of the mother as possible.

3. Promote infant-mother bonding by allowing baby visitations in the ICU as soon as the conditions of mother and infant stabilize. Allow mother to feed baby if possible. Maintain infant safety if mother’s condition is marginally stable.

4. Discuss feelings about labor, delivery, and complications with patient and family members. Relay information about the condition of the infant as often as possible, if mother is unable to visit with the baby.

5. If the infant or mother expires, provide all possible support measures for the patient and significant others, including pastoral care and referrals to community support groups or professional counseling.

Family Involvement Promotion; Family Process Maintenance; Normalization Promotion

Oncologic emergencies

An oncologic emergency is defined as a life-threatening situation occurring as a manifestation of a malignancy or the result of antineoplastic treatment or tumor progression. Such emergencies most commonly arise from the ability of cancer to (1) spread by direct infringement on adjacent structures or metastasize to distant sites leading to thrombosis or hemorrhage, (2) produce abnormal amounts of hormones or cellular products leading to fluid and electrolyte imbalances and organ failure, (3) infiltrate serous membranes with effusion, (4) obstruct vessels, ducts, or hollow viscera, or (5) replace normal organ parenchyma. As more aggressive therapies are used in the treatment of these cancers, side effects are more intense and the use of critical care to manage such side effects will only increase.

Early recognition and intervention are essential to enhance positive outcomes. Once an oncologic emergency is recognized, the aggressiveness of management is influenced by the reversibility of the immediate situation, the probability of long-term survival, and the ability to provide effective supportive care.

Oncologic emergencies can be classified as hematologic, structural, metabolic, or side effects from treatment such as chemotherapy, radiation therapy, biologic therapy, surgery, or bone marrow transplantation. Neutropenic sepsis, tumor lysis syndrome (TLS), and superior vena cava syndrome (SVCS) will be discussed in this chapter as examples of oncologic emergencies seen in the critical care arena. When recognized early and managed appropriately, these acutely ill individuals have a high likelihood of recovery. An overview of additional oncologic emergencies, associated causes, and signs and symptoms is given in Table 11-8.

Table 11-8 ONCOLOGIC EMERGENCIES DEFINED

Cancer patients may require intensive care for several reasons: (1) overwhelming infection and sepsis, (2) structural complications of cancer or cancer treatment, or (3) metabolic complications of cancer or cancer treatment. Intensivists sometimes refuse admission to cancer patients needing critical care, which may result in denial of effective care for some deserving patients. A cancer patient may need admission to intensive care units for a variety of reasons. The outcomes of patients with hematologic malignancies, previously dismal, have improved over the last 10 years. The previously known indicators of poor outcome are no longer valid in view of recent advances in intensive care. A select group of patients with hematologic malignancies may be offered aggressive therapy for a limited duration and then prognosis can be reassessed. Cancer chemotherapy can produce toxicities affecting all major organ systems. Such patients may be admitted with acute organ dysfunction or years afterward for incidental illnesses. Knowledge of these toxicities is essential for early diagnosis, management, and prognostication in such patients. The postsurgical cancer patient has unique problems; the problems of these groups are discussed. The postsurgical cancer patient may need care ranging from monitoring alone after major surgery in some patients, to fully aggressive intensive care for postsurgical anastomotic dehiscence, mediastinitis, septic shock, and multiorgan dysfunction in others. The metabolic and mechanical complications commonly seen in nonsurgical cancer patients are also reasons for admission. Intensive care should be offered to all patients who have a reasonable chance of cure or supportive care of their disease. The intensivist must be able to recognize the potentially reversible critical illness among the various groups of cancer patients and discourage admission to terminally ill cancer patients. The intensivist must also be aware that the alleviation of the suffering in the last hours of the life of a terminal cancer patient is one of the functions of an ICU, once a decision to discontinue aggressive therapy has been taken, if there isn’t time for transfer to a hospice.

neutropenic sepsis

Pathophysiology

Neutropenia is defined as an abnormally low level of neutrophils in the blood. The normal level of neutrophils in human blood varies slightly by age and race. Infants have lower counts than older children and adults, and African Americans have lower counts than do whites or Asians. The average adult level is 1500 cells/mm³ of blood. Neutrophil counts (in cells/mm³) are interpreted as follows:

• Greater than 1000—Normal protection against infection

• 500 to 1000—Some increased risk of infection

• 200 to 500—Great risk of severe infection

• Lower than 200—Risk of overwhelming infection; requires hospital treatment with antibiotics

Untreated bacteremia in patients with neutropenia is fatal: septic shock is associated with a 50% to 70% mortality rate. Mortality is associated with causative organism, site of infection, and the level and duration of neutropenia. The risk of infection is greater the faster the rate of decline of the neutrophil count and the longer the duration of neutropenia, especially if neutropenia lasts longer than 10 days. Infections in neutropenic patients typically take 2 to 7 days to respond to antimicrobial therapy. Fever (or any inflammatory response related to white cells or cytokines) may not be present in some infected neutropenic patients who are dehydrated or taking steroids or NSAIDs, and the possibility of infection must be considered in any neutropenic patient who is unwell.

Asssessment: neutropenic sepsis

History and risk factors

Granulocytopenia, immunosuppression, recent cancer treatment, diabetes, organ-related disease, age greater than 65 years, indwelling catheters, long hospital or ICU stays, loss of skin or mucosal integrity, malnutrition, hypothermia, intubation/mechanical ventilation, aspiration, alcoholism, renal failure, hepatic failure, chronic illness. The risk of death is twice as great for sepsis patients with cancer as for those without and is comparable to the risk observed in sepsis patients who are HIV positive.

The four stages of sepsis

The progression of sepsis is subtle, rapid, and often deadly and usually broken down into four stages.

Stage 1.

Systemic inflammatory response syndrome (SIRS) describes a systemic inflammation without a defined source of infection resulting from any major insult to the body, such as trauma, burns, or myocardial infarction, in which two or more of the following are present:

• HR at least 90 bpm

• Body temperature less than 36°C (96.8°F) or greater than 38°C (100.4°F)

• Tachypnea greater than 20 breaths/min or, on blood gas, a PaCO₂ less than 32 mm Hg

• WBC less than 4000 cell/mm³ or greater than 12,000 cells/mm³ or the presence of greater than 10% immature neutrophils

Patients with SIRS can be routinely cared for on the medical-surgical floor but should be closely monitored for signs and symptoms of sepsis.

Stage 2.

Sepsis is identified by the presence of two of the SIRS criteria in response to pathogenic microorganisms and associated endotoxins in the blood. However, in many cases of sepsis, the actual cause of infection is never identified. The delay in waiting for confirmation of infection can slow the treatment of sepsis; the most effective course of action once SIRS is identified and infection is suspected is to treat the infection and monitor the patient for signs and symptoms of organ failure, which will indicate that the condition has progressed to severe sepsis.

Stage 3.

Severe sepsis occurs when a patient who meets the sepsis criteria shows one of the signs and symptoms of organ failure. Once severe sepsis is suspected, the patient requires aggressive treatment in a critical care area.

Stage 4.

Septic shock is defined as severe sepsis plus hypotension (a systolic BP less than 90 mm Hg) that does not respond to fluid resuscitation. Septic shock is associated with a high mortality rate. The patient’s chances of recovery are significantly reduced if, by this stage of sepsis, she or he has not already been transferred to the ICU.

Observation: rapid progression if untreated

Signs and symptoms of infection may be absent due to decreased WBCs.

• General: fever, hypothermia, chills, pain

• Neurological: confusion, anxiety, restlessness, decreased level of consciousness, coma

• Pulmonary: tachypnea, rales, rhonchi, wheezes, dry cough, cyanosis, hypoxia, ARDS

• Cardiovascular: tachycardia, hypotension, fluctuating pulse pressure, thready pulse

• Digestive: nausea, vomiting, anorexia, decreased GI motility, GI bleed

• Renal: decreased urine output, anuria, renal failure

• Integument: warm, flushed changing to damp, cool, clammy

Diagnostic Tests for Neutropenic Sepsis

Test	Purpose	Abnormal Findings
Blood cultures (done baseline and every 24 hours if signs and symptoms of sepsis persist)	Check for bacteria or other microorganisms in a blood sample.	Gram-positive cocci: coagulase-negative staphylococci, Viridans streptococci and Staphylococcus aureus Gram-negative pathogens: Escherichia coli, Klebsiella spp., and Pseudomonas aeruginosa. Fungal: Candida spp., Aspergillus spp. Viral: Herpes simplex; respiratory syncytial virus
Cultures (throat, stool, urine, CV catheter, other sites of exudates) prior to antibiotics to determine pathogen	Determines source of infection	As above
Chest radiographic examination	Evaluates lung status	Pulmonary infiltrates, pulmonary edema
Complete blood count (CBC)	Evaluates the composition and concentration of the cellular components of blood	Increased WBC with infection, decreased WBC with sepsis; chemotherapy, radiation, leukemias
Chemistries – electrolytes, liver function tests	Evaluates blood chemistries and liver function	Increased BUN, creatinine reveal dehydration; Increase to decrease in glucose due to shock; increased transaminase, bilirubin, serum lactate in sepsis due to shock
Coagulation profile	Examines the factors most often associated with a bleeding problem	Prolonged PT, PTT
Pulse oximetry, ABGs	Measures oxygenation, acid-base balance	Respiratory alkalosis followed by metabolic acidosis
Electrocardiogram	Records the electrical activity of the heart.	Tachycardia, arrhythmias

Collaborative management

Fever (even low grade) is often the only reliable sign of infection in the neutropenic patient. No specific patterns of fever or clinical features can positively distinguish between fever due to infection and one of noninfectious cause. Therefore, all febrile neutropenic patients should be considered for the administration of empirical broad-spectrum antibiotics within 1 hour of presentation. Many patients are outpatients during their cancer treatments, and it is vital to their survival that they and their significant others be educated about early recognition (and timing during treatment) of neutropenia to minimize the risk of sepsis. All health care providers should be educated about this potential life-threatening situation and be aware of strategies to minimize risk to patients by systematically and regularly evaluating response to treatment and progress toward desired outcomes.

Because sepsis-related mortality is unacceptably high, the Society of Critical Care Medicine (SCCM) set a quality improvement goal to reduce mortality caused by severe sepsis and septic shock by 25%. Clearer definitions of sepsis, severe sepsis, and septic shock will help in achieving this goal, as will recently updated evidence-based management guidelines for severe sepsis and septic shock. To be effective, these definitions and guidelines need to be applied to the early identification and aggressive treatment of patients who have severe sepsis or septic shock. Early goal-directed therapy to achieve hemodynamic stabilization has been demonstrated to decrease mortality in patients who have septic shock. See SIRS, Sepsis and MODS, p. 927.

Care priorities

1. Manage hypovolemia:

Once severe sepsis or septic shock has been identified, the highest management priorities are to establish vascular access and initiate fluid resuscitation to improve tissue perfusion. Failure to manage global hypoxia can lead to MODS. Fluid resuscitation guidelines are defined by the Society of Critical Care Medicine and are a part of early goal-directed therapy (see Sepsis, SIRS, and MODS, p. 927).

2. Restore tissue oxygenation:

Measurements commonly used are SvO₂, ScvO₂, and lactate levels. Low values indicate several possible causes of poor oxygenation, including inadequate oxygen delivery, high oxygen demand, or inability of tissues to extract oxygen from hemoglobin (see Sepsis, SIRS, and MODS, p. 927).

3. Identify and manage the underlying infection:

Selection of an appropriate antimicrobial agent, often in the absence of microbiologic confirmation, requires consideration of patient-related characteristics such as drug intolerances, recently used antibiotics, previous infections, underlying disease, and clinical syndrome. Awareness of the prevalence of infections caused by specific organisms can provide clinicians with insight into appropriate empiric antimicrobial therapy. Pathogen resistance patterns in the hospital and community, along with hospital protocols to limit antibiotic resistance, also should be considered.

CARE PLANS FOR NEUTROPENIA

Ineffective protection: potential for life-threatening infections

No fever, no clinical signs or symptoms of sepsis, no growth in blood, excrement or skin surface cultures

Immune Status

Infection control

1. Assess for signs and symptoms of infection, sepsis, septic shock.

• Monitor temperature every 2 to 4 hours.

• Monitor vital signs frequently for signs of impending shock: increased HR and RR, increased restlessness and anxiety, and cool and clammy skin, followed by a decrease in BP.

• Monitor WBC and differential for evidence of infection and response to interventions.

• Auscultate breath sounds for adventitious sounds or diminished breath sounds.

• Observe all dressing sites daily for signs and symptoms of infection.

• Observe all orifices daily for evidence of localized infection.

• Assess areas of localized pain for erythema, swelling, exudate, or rebound tenderness.

2. Control environmental risks of infection

• Strict handwashing.

• Universal precautions.

• Do not assign neutropenic patients with those known to be infected.

• Monitor visitors for recent history of communicable disease and institute precautions as needed.

• Clean all multipurpose equipment between patient use.

• No live flowers kept in standing water.

3. Implement patient care routines to minimize infection,

• Assist with daily bathing, oral and perineal hygiene; change linens daily.

• Ensure sleep and nutritional needs are met to promote immune system recovery.

• Sterile technique for insertion and care of IV catheters.

• Encourage incentive spirometry or deep breathing and coughing.

• Encourage ambulation if patient is able or turn every 2 to 4 hours to minimize skin breakdown or atelectasis.

Cardiac Care: Acute; Circulatory Care: Arterial Insufficiency; Respiratory Monitoring; Shock Management: Cardiac; Cerebral Perfusion Promotion; Neurologic Monitoring; Fluid/Electrolyte Management; Vital Signs Monitoring

Decreased cardiac output

Patient will have normal BP; patient will exhibit signs of adequate tissue perfusion as evidenced by adequate urinary output and normal mental status.

Circulation Status

Hypovolemia management

1. Monitor I&O hourly. Consult physician for a urinary output less than 0.5 ml/kg/hr for 4 consecutive hours. Insert urinary catheter if appropriate.

2. Monitor and document HR, rhythm, pulses, and BP.

3. Evaluate efficacy of volume expansion by closely comparing CVP, PAWP, and CO. Overzealous volume expansion can lead to heart failure and pulmonary edema.

4. Administer diuretics as prescribed in the well-hydrated patient with urine output less than 0.5 ml/kg/hr.

5. Assess patient for volume depletion, including poor skin turgor; dry mucous membranes; hypotension; tachycardia; and decreasing urine output, CVP, and CO.

6. Monitor electrolytes and serum osmolality. A universal increase in electrolytes and osmolality is indicative of dehydration. A universal decrease signals fluid overload.

7. Assess pH (normal range is 7.35 to 7.45) before replacing electrolytes. Acidosis and alkalosis alter electrolyte values. Replace potassium if the pH is outside the normal range.

Electrolyte Monitoring; Fluid Management; Fluid Monitoring; Intravenous (IV) Therapy; Hypervolemia Management; Shock Management: Volume

Acute pain