Complex special situations

CHAPTER 11 Complex special situations

“. . . the end result of a progressive, unchecked increase in intra-abdominal pressure from a myriad of disorders that eventually leads to multiple organ dysfunction.”

John Hunt, MD

Pathophysiology

Intra-abdominal hypertension (IAH) occurs when the amount of intra-abdominal contents (through edematous bowel or fluid accumulating in the cavity) exceeds the distendable capability of the fascia. The result is an intra-abdominal hypertensive state. which can lead to abdominal compartment syndrome (ACS). As the fluid accumulates (due to bleeding, ascites, volume overload, and other causes), the resulting increase in pressure (change in compliance/change in volume) initially affects regional blood flow and results in impaired tissue perfusion, which is then associated with a systemic inflammatory response. The resulting ischemia and inflammatory response further causes capillary leakage and compression of the intra-abdominal viscera. If untreated, the continually elevated free fluid and measured pressure begin to compress blood vessels, causing organ dysfunction both inside and outside the abdomen, and lead to abdominal compartment syndrome. The inflammatory response promotes the release of cytokines, causing vasodilation and cell membrane dysfunction. The cell membrane loses integrity, which causes further inflammation, profound edema and ultimately cell death. The elevated pressure in the abdominal cavity generated by the severe increase in extra vascular fluid load increases the intra-abdominal contents (free water) and further impairs intestinal tissue perfusion as compression of the arteries and veins continues. This process underlies the multi-organ effects of rising intra-abdominal pressure (IAP). When the IAP rises above critical level, blood flow to the abdominal viscera and organs decreases and ACS is imminent.

Definitions

IAP refers to the pressure present within the abdominal cavity. The pressure within the cavity reflects the presence of extravascular fluids, which compress the blood vessels and organs in the abdominal cavity as well as displacing the diaphragm into the thoracic cage, which limits lung expansion. Elevated intrabladder pressure indirectly reflects high pressure within the abdominal cavity.

IAH is defined by the World Society of Abdominal Compartment Syndrome (WSACS) as a measured IAP of 12 mm Hg or greater, recorded three times using standardized measurement methods 4 to 6 hours apart and/or an abdominal perfusion pressure (APP) of less than 60 mm Hg (mean arterial pressure [MAP] minus intra-abdominal bladder pressure [IABP]), recorded using two standardized measurements 1-6 hours apart). These measurements should be evaluated in the context of clinical symptomatology.

An IAP of greater than 20 mm Hg reflects significant IAH almost universally.

An IAP of 18 mm Hg indicates a high probability of organ compromise.

An IAP of 15 mm Hg reflects moderate probability of organ compromise.

An IAP of 12 mm Hg reflects a lower probability of organ compromise.

Increased IAP may reflect a critical finding in patients with multiorgan dysfunction syndrome (MODS) or multisystem failure, which contributes to global hypoperfusion, aggravating the effects of increased IAP (Table 11-1).

Table 11-1 PRESSURE AND SYMPTOM GRADE FOR INTRA-ABDOMINAL HYPERTENSION

Graded Measurement	Pressure Measurement and relevance	Physiologic Events and clinical signs
Pressure Grade I	12–15 mm Hg Significant in the presence of organ dysfunction	Cytokine release and capillary leak Third spacing of resuscitative fluid Decreasing venous return and preload Early effects on ICP and CPP Abdominal wall perfusion decreases 42% Marked reduction in intestinal and intra-abdominal organ blood flow leading to regional acidosis and free radical formation.
Pressure Grade II	16–20 mm Hg Significant in most patients	Markedly decreased venous return, CO and splanchnic perfusion Increased SVR, CVP, PAWP Decreased blood pressure, pulse pressure and particularly systolic blood pressure Decreased TLC, FRC, RV. Increased vent pressures, hypercapnia, hypoxia Reduction to 61% of baseline mucosal blood flow and increasing gut acidosis Oliguria, anuria Increasing ICP and decreasing CPP
Pressure Grade III	21–25 mm Hg Significant in all patients	Hemodynamic collapse, worsening acidosis, hypoxia, hypercapnia, anuria. Inability to oxygenate, ventilate or resuscitate
Pressure Grade IV	>25 mm Hg Significant in all patients	Hemodynamic collapse, worsening acidosis, hypoxia, hypercapnia, anuria. Inability to oxygenate, ventilate or resuscitate

If both pressure and clinical symptoms are met for grade III and/or grade IV, patient has abdominal compartment syndrome.

ACS is defined as “intra-abdominal hypertension with a gradual and consistent increase in the IAP value of [equal to or greater than] 20 mm Hg,” recorded by at least three standardized measurements taken 1 to 6 hours apart and in conjunction with at least one new onset organ dysfunction. ACS can be fatal and often complicates or results in a clinical condition refractory to treatment. The astute clinician suspects IAH and ACS when MODS is evolving and/or the patient presents with persistent lactic acidosis.

Historically, the belief of most critical care providers was that IAH and the more serious evolution of the state, ACS, was solely related to traumatic injury of the abdomen, including surgery. Within the last decade, the understanding of the pathophysiology involved in developing IAH and ACS has been enhanced by studies and revealed the prevalence in all critical patients; medical as well as surgical and trauma. The progressive conditions have been divided into two categories: primary or secondary abdominal hypertension disorders. The causes may differ, but outcomes are similar if either condition remains untreated.

Primary ACS is a condition associated with injury or disease in the abdominopelvic region that frequently requires early surgical or angioradiologic intervention. Any abnormal event that raises abdominal pressure can induce acute IAH, including blunt or penetrating abdominal trauma, abdominal aortic aneurysm (AAA), hemorrhagic pancreatitis, gastrointestinal (GI) obstruction, abdominal surgery resulting in retroperitoneal bleeding or secondary peritonitis, and with tight closure of abdominal incisions. Primary ACS also includes patients with abdominal solid organ injuries who were initially managed medically and then developed ACS. The condition has been relatively well understood by surgeons and their colleagues but is frequently misdiagnosed and/or untreated until surgical intervention is required.

Secondary ACS includes conditions that do not originate from abdominal injury that create IAH, including sepsis or any condition prompting capillary leak (e.g., major burns, and conditions requiring massive fluid resuscitation). A large multicenter study (Malbrain et al. 2005) found the prevalence of IAH was 54% among medical ICU patients and 65% in surgical ICU patients. This was remarkable, as most medical patients are not evaluated for or even considered recipients of IAH and ACS.

ACS treatments are the same regardless of the cause; however, the caregiver must be very careful in managing secondary ACS. The opportunity for early intervention may be lost with the subtle development of signs and symptoms of IAH and ACS. The lack of definitive signs often leads to delayed diagnosis and delayed recognition, and an urgent medical condition becomes an emergency surgical situation. Increased organ failure, increased mortality, increased resource utilization, and longer ICU lengths of stay may result. Similar to sepsis and severe sepsis, the greatest challenge is early recognition and diagnosis. Monitoring all high-risk patients would enable clinicians to trend the IAP, facilitating early, appropriate interventions when the syndrome is more likely to be responsive to medical therapy. The best management strategy is to prevent abdominal compartment syndrome via early monitoring, early medical interventions, and early surgical decompression if needed.

Assessment

Diagnostic tests

Methods of intra-abdominal pressure measurement

The best method for measurement of IAP is controversial. The most common method is measuring the response of intra-bladder compliance to an instillation of 25 ml of sterile fluid by measuring the resulting pressure.

Direct intraperitoneal measurement:

The most accurate method requires an intraperitoneal catheter inserted into the abdomen with a fluid manometer or pressure transducer attached to measure the pressure. This method requires expert catheter placement and is highly linked to infection.

Indirect methods:

Bladder pressure is commonly used, while other methods are infrequently used. Indirect methods include gastric pressure measurement through gastrostomy or a nasogastric tube, intrarectal pressure measurement using an esophageal stethoscope catheter, or bladder pressure measurement through a urinary catheter.

Bladder pressure measurement:

An indwelling urinary catheter is connected to either a pressure transducer or a fluid manometer to measure the pressure. Readings are reliable and easier to perform than direct intraperitoneal measurement.

The urinary bladder normally has a compliant wall. Many studies reveal compliance decreases when there is a high presence of intra-abdominal fluids, which increase the pressure in the abdominal cavity and compress the bladder, increasing resistance. When fluid is injected into the bladder pressure system, any decrease in bladder compliance is reflected by increased intra-bladder pressure. The procedure is generally easier and safer if a prepackaged closed bladder pressure system is used. If assembling the system without a prepackaged tool, use the urinary/Foley catheter with an aspiration or infusion port:

1. The nurse will connect a fluid filled pressure system to a transducer, then connect a needle to the distal end of the tubing (farthest from the transducer and after a stopcock).

2. The cable connecting the system to the monitor should allow for visualization of a small pressure (scale either auto or at 30 mm Hg).

3. The connected system will be inserted into the catheter infusion port.

4. After zeroing the system (transducer at the symphysis pubis and the stopcock will be turned off to the patient), the nurse will clamp the catheter drainage system just below the infusion port.

5. Using the stopcock, the system will be turned off to the monitor and 25 mls of sterile fluid (IV fluid is fine) will be injected rapidly into the infusion port on the urinary catheter. The stopcock will be then turned off to the injecting port, leaving a connected pressure system from patient to monitor.

6. Bladder pressure must be read during end expiration and the patient must be as flat as tolerated to facilitate accuracy. There is no dynamic waveform associated with bladder pressure. One should just observe the level of pressure in the first 10–20 seconds after fluid is instilled.

7. A normal value is generally considered between 0 and 5 mm Hg, although levels as high as 15 mm Hg are not unusual in the first 24 hours after abdominal surgery (see Table 11-1). If the pressures are elevated, document and repeat in the next hour using the same techniques. Inform the physician or midlevel practitioner if both measures are elevated.

8. Occlusion is then released and fluid is drained into the urine collection bag. Subtract the amount of fluid from the hourly output.

Collaborative management

Care priorities

1. Prevent abdominal compartment syndrome:

Patients who have a high index of suspicion should have bladder pressure monitoring initiated in order to identify IAH earlier and possibly avoid decompressive laparotomy, which is the only documented evidence-based therapy for ACS (Box 11-1). There are many approaches that may be used to reduce IAH. These strategies are directed at reducing increased abdominal cavity volume or decreasing compliance. Therapies include:

Box 11-1 MANAGEMENT OF ABDOMINAL COMPARTMENT SYNDROME

1. Improvement of abdominal wall compliance

• Sedation

• Pain relief (Do not use fentanyl!)

• Neuromuscular blockade

• Body positioning

• Negative fluid balance

• Percutaneous abdominal wall component separation

2. Evacuation of intraluminal contents

• Nasogastric suction

• Rectal tube/enemas

• Gastro/colonic prokinetic agents

• Paracentesis

• Percutaneous drainage of abscess/hematomas

3. Evacuation of peri-intestinal and abdominal fluids

• Ascites evacuation in cirrhosis

• CT- or US-guided aspiration of abscess

• CT- or US-guided aspiration of hematoma

• Percutaneous drainage of (blood) collections

4. Correction of capillary leak and positive fluid balance

• Diuretics/colloids/hypertonic fluids

• Hemodialysis/ultrafiltration

• Dobutamine (Do not use dopamine!)

• Ascorbic acid in burn patients

CT, computerized tomography; US, ultrasound.

Modified from Ivatury et al: In Vincent JL, editor: Yearbook of intensive care and emergency medicine. Berlin, 2008, Springer, p. 554.

Draining free intraperitoneal fluid:

Paracentesis is performed by the advanced practitioner. Some centers may place a peritoneal drainage catheter and leave it in place if abdominal fluid accumulation is persistent and severe.

Volume replacement with small volumes of higher osmotic gradient IV fluids:

More highly concentrated IV solutions (e.g., hypertonic [3%] saline, plasma, hextend, blood products) can sometimes facilitate fluid stabilization within the vasculature for longer periods of time than isotonic solutions.

Continuous renal replacement therapy (crrt):

Enables minute-to-minute control of intravascular fluid removal and replacement. Fluid management is more exact and CRRT was thought to benefit the patient by removal of cytokines, but more recent evidence indicates that may not be of benefit (see Continuous Renal Replacement Therapies, p. 603).

Other options:

Include the sedation and analgesic management of patients and ultimately the consideration of neuromuscular blockade or chemical paralysis

2. Perform a decompressive laparotomy to relieve acs:

Sudden release of the abdominal pressure may lead to further complications including ischemia-reperfusion injury, acute vasodilation, cardiac dysfunction, and arrest. Arteries and veins within the abdomen are suddenly able to expand to normal size and “refill” with normal blood volume. If the patient has insufficient volume to accommodate the renewed space within the vasculature, hypotension ensues. Patients should be hydrated with at least 2 L of intravenous (IV) fluid, which may include a “cellular protection cocktail,” such as 25 grams of mannitol 12.5% given along with 2 ampules of bicarbonate per liter. IV fluids and vasopressors should be immediately available in case severe hypotension occurs as the abdomen is decompressed.

After opening the abdomen, temporary closure will be applied. The goal is to permanently close the abdomen as soon as possible. For most patients who require emergent opening of the abdomen for ACS, a vacuum-assisted closure device (abdominal wound VAC) attached to a negative pressure device is commonly applied. An open abdomen may precipitate loss of liters of volume. The modified negative pressure wound VAC facilitates open wound fluid and management and supports granulation of tissue, as well as local perfusion, which facilitates eventual closure of the open wound.

11-1 RESEARCH BRIEF

Tremblay and colleagues reported on 181 patients with an open abdomen over a 4-year period managed with silos, skin only or towel clip closure, open packing, and modified visceral packing—in fact, anything other than vacuum-assisted closure (VAC). Mortality and other complications were extremely high in this group compared to those with VAC: 14% developed enterocutaneous fistulas, 5% suffered wound dehiscence, and almost half of the patients in the series were left with large incisional hernias at discharge. The study concluded some method of vacuum-assisted technique should be applied in the majority of patients.

Tremblay LN, Feliciano DV, Schmidt J, et al: Skin only or silo closure in the critically ill patient with an open abdomen. Am J Surg 182:670, 2001.

CARE PLANS FOR ABDOMINAL COMPARTMENT SYNDROME AND INTRA-ABDOMINAL HYPERTENSION

Deficient fluid volume

Goals/outcomes

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

Goals/outcomes

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

Goals/outcomes

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.

Routes of administration:

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

Collaborative management

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

Collaborative management

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

Street names:

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

Routes of administration:

Oral, IV, IM, intranasal, smoked

Collaborative management

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.

Prevention/treatment of seizures:

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.

Street names:

Yellow jackets, reds, barbs

Routes of administration:

Oral, IV, IM

Collaborative management

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.

Prevention/treatment of seizures:

Phenytoin or diazepam may be given.

Sedation for withdrawal symptoms:

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

Prevention of aspiration:

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