Browse the corpus

Specific Critical Care Topics anesthetic agents (such as halothane and isoflurane) or the TIIBLE 64. Symptoms and Signs of Hypothermia depolarizing paralytic succinylcholine. Exposure to one of Severity Core Findings these agents may result in muscle rigidity, rhabdomyolysis, Temperature cardiac arrhl'thmias, and core body temperature elevation to Mild 32.0-35.0 "c t HR, t BB 1 RR, shivering, 45 'C (113 oF) or greater. Mortality can reach 10%. Treatment (89.6-9s.0'F) alert, poor judgment consists of discontinuing the triggering agent, active cooling, Moderate 28.0-32.0'C J HR, J BB J RR, J CO, JO, and administration of the muscle relaxant dantrolene every 5 (82.4-89.6"F) consumption, J kidney function, somnolence, no to 10 minutes until muscle rigidity and hyperthermia resolve. shivering, supraventricu lar arrhythmia Neuroleptic Malignant Syndrome and Severe <28.0 "C Coma, absent reflexes, Serotonin Syndrome (<82.4"F) ventricular arrhythmia, Neuroleptic malignant syndrome is an idiosyncratic response asystole, apnea

anesthetic agents (such as halothane and isoflurane) or the TIIBLE 64. Symptoms and Signs of Hypothermia depolarizing paralytic succinylcholine. Exposure to one of Severity Core Findings these agents may result in muscle rigidity, rhabdomyolysis, Temperature cardiac arrhl'thmias, and core body temperature elevation to Mild 32.0-35.0 "c t HR, t BB 1 RR, shivering, 45 'C (113 oF) or greater. Mortality can reach 10%. Treatment (89.6-9s.0'F) alert, poor judgment consists of discontinuing the triggering agent, active cooling, Moderate 28.0-32.0'C J HR, J BB J RR, J CO, JO, and administration of the muscle relaxant dantrolene every 5 (82.4-89.6"F) consumption, J kidney function, somnolence, no to 10 minutes until muscle rigidity and hyperthermia resolve. shivering, supraventricu lar arrhythmia Neuroleptic Malignant Syndrome and Severe <28.0 "C Coma, absent reflexes, Serotonin Syndrome (<82.4"F) ventricular arrhythmia, Neuroleptic malignant syndrome is an idiosyncratic response asystole, apnea classically associated with first-generation antipsychotic blood pressure; CO = cardiac output; HR = heart rate; RR = respiration rate. agents such as haloperidol, but it is also seen with newer generation antipsychotics as well as antiemetics. It is more common at times of initiation or dose escalation but can occur arrhythmias, and further depression of mental status with after prolonged use. Highlighting a potential pathogenetic role eventual coma (Table 64). In moderate to severe hypothermia, lor dopamine receptor blockade, it has also been described Osborne waves may be present on electrocardiogram tracings after rapid withdrawal of dopaminergic medications for (Figure 29). Parkinson disease. The syndrome is characterized by the tetrad If a severely hypothermic patient becomes pulseless and of fever, mental status changes, muscle rigidity, and dysauto requires resuscitation, it is reasonable to continue cardiopul nomia. Mortality may exceed 10'1,. Treatment includes stop- monary resuscitation for a prolonged period until the patient ping the triggering agent (or reinstating the withdrawn dopa can be rewarmed. There are reports of cardiopulmonary minergic agent), active cooling, and supportive care including resuscitation lasting hours and resulting in full recovery when IV fluid administration. Evidence for pharmacotherapy is a severely hypothermic patient has a cardiac arrest. anecdotal, but options include benzodiazepines, dantrolene, Hypothermic patients who are shivering will passively and bromocriptine. Neuroleptic medications can be reintro rewarm themselves if they are removed from the cold environ duced after a waiting period of at least 2 weeks, usually at ment and given adequate insulation to prevent heat loss. As lower dose. with care to avoid dehydration and concomitant core temperature drops below 32 'C (89.6 'F) and shivering administration with lithium. stops, active rewarming should be implemented to prevent Serotonin syndrome can present with mental status complications. Such techniques include surface methods, changes, dysautonomia, hyperthermia, hyperreflexia, and other such as heating pads and forced-air warming systems, as well muscle abnormalities. It is most commonly associated with as invasive methods such as rewarming by peritoneal or pleu- selective serotonin reuptake inhibitors, but other drugs that ral space irrigation using peritoneal catheters or thoracostomy affect serotonin signaling have been implicated. I\4anagement tubes. Extracorporeal support, including cardiopulmonary includes removing the olfending agent and supportive care. bypass, is recommended lor patients in cardiac arrest because Cyproheptadine is sometimes used off label if benzodiaz it maximizes the rewarming rate and can provide hemody epines fail to control symptoms. namic support. During active rewarming, core temperature should be monitored with an esophageal temperature probe. I(EY POIilT as rectal and bladder temperatures will lag behind the rising r Treatment of neuroleptic malignant syndrome includes core temperature during the rewarming process. stopping the triggering agent, active cooling, and rehy- dration. Toxicology Alcohol Poisoning Accidenta I Hypothermia Ethanol and other ingested alcohols activate the y-aminobutyric Accidental hypothermia, defined by a core temperature below acid receptor, which is the primary central nervous system 35 'C (95 'F), is classically associated with winter in cold cli mates but can occur in more temperate weather if the exposure 1,..! is sufficient (such as in wet conditions). In mild hypothermia, shivering is an effective compensatory mechanism, but in more severe cases (core temperature lower than 32 'C [89.6 "F]), ,I I it eventually ceases. Early signs of hypothermia include tachy FIGURE 29. Electrocardiogram showing Osborne waves associated with cardia, hyperventilation, poor judgment, and diuresis. Later hypothermia. Ihey are best seen in lhe inferior and lateral chest leads. 0sborne findings include hypotension, bradycardia and other cardiac waves are defined by the shoulder or "hump" between ORS and SI segments.

classically associated with first-generation antipsychotic blood pressure; CO = cardiac output; HR = heart rate; RR = respiration rate. agents such as haloperidol, but it is also seen with newer generation antipsychotics as well as antiemetics. It is more common at times of initiation or dose escalation but can occur arrhythmias, and further depression of mental status with after prolonged use. Highlighting a potential pathogenetic role eventual coma (Table 64). In moderate to severe hypothermia, lor dopamine receptor blockade, it has also been described Osborne waves may be present on electrocardiogram tracings after rapid withdrawal of dopaminergic medications for (Figure 29). Parkinson disease. The syndrome is characterized by the tetrad If a severely hypothermic patient becomes pulseless and of fever, mental status changes, muscle rigidity, and dysauto requires resuscitation, it is reasonable to continue cardiopul nomia. Mortality may exceed 10'1,. Treatment includes stop- monary resuscitation for a prolonged period until the patient ping the triggering agent (or reinstating the withdrawn dopa can be rewarmed. There are reports of cardiopulmonary minergic agent), active cooling, and supportive care including resuscitation lasting hours and resulting in full recovery when IV fluid administration. Evidence for pharmacotherapy is a severely hypothermic patient has a cardiac arrest. anecdotal, but options include benzodiazepines, dantrolene, Hypothermic patients who are shivering will passively and bromocriptine. Neuroleptic medications can be reintro rewarm themselves if they are removed from the cold environ duced after a waiting period of at least 2 weeks, usually at ment and given adequate insulation to prevent heat loss. As lower dose. with care to avoid dehydration and concomitant core temperature drops below 32 'C (89.6 'F) and shivering administration with lithium. stops, active rewarming should be implemented to prevent Serotonin syndrome can present with mental status complications. Such techniques include surface methods, changes, dysautonomia, hyperthermia, hyperreflexia, and other such as heating pads and forced-air warming systems, as well muscle abnormalities. It is most commonly associated with as invasive methods such as rewarming by peritoneal or pleu- selective serotonin reuptake inhibitors, but other drugs that ral space irrigation using peritoneal catheters or thoracostomy affect serotonin signaling have been implicated. I\4anagement tubes. Extracorporeal support, including cardiopulmonary includes removing the olfending agent and supportive care. bypass, is recommended lor patients in cardiac arrest because Cyproheptadine is sometimes used off label if benzodiaz it maximizes the rewarming rate and can provide hemody epines fail to control symptoms. namic support. During active rewarming, core temperature should be monitored with an esophageal temperature probe. I(EY POIilT as rectal and bladder temperatures will lag behind the rising r Treatment of neuroleptic malignant syndrome includes core temperature during the rewarming process. stopping the triggering agent, active cooling, and rehy- dration. Toxicology Alcohol Poisoning Accidenta I Hypothermia Ethanol and other ingested alcohols activate the y-aminobutyric Accidental hypothermia, defined by a core temperature below acid receptor, which is the primary central nervous system 35 'C (95 'F), is classically associated with winter in cold cli mates but can occur in more temperate weather if the exposure 1,..! is sufficient (such as in wet conditions). In mild hypothermia, shivering is an effective compensatory mechanism, but in more severe cases (core temperature lower than 32 'C [89.6 "F]), ,I I it eventually ceases. Early signs of hypothermia include tachy FIGURE 29. Electrocardiogram showing Osborne waves associated with cardia, hyperventilation, poor judgment, and diuresis. Later hypothermia. Ihey are best seen in lhe inferior and lateral chest leads. 0sborne findings include hypotension, bradycardia and other cardiac waves are defined by the shoulder or "hump" between ORS and SI segments. 82

Specific Critical Care Topics TABLE 65. Presentation and Treatment of Alcohol Poisoning Alcohol Common Sources Major Findings Anion Gap Osmolar Gap Antidote Ethanol Alcoholic beverages CNS depression Possible Yes Supportive care Nausea, emesis lsopropyl Rubbing alcohol CNS depression No Yes Supportive care alcohol Disinfectants Ketone elevation Antifreeze Methanol Windshield wiperfluid CNS depression Yes Yes Fomepizole De-icing solutions Vision loss Ethanol (only if fomepizole is not available) Solvents Hypotension HD {or severe acidemia, very "Moonshine" large ingestions, severe CNS depression, and any visual impairment Ethylene Antifreeze CNS depression Yes Yes Fomepizole glycol De-icing solutions AKI Ethanol (only if fomepizole is not available) Solvents Hypocalcemia HD for severe acidemia, very Hypotension large ingestions, severe CNS depression, AKl, and systemic collapse AKI = acute kidney injury; CNS = central nervous system; HD = hemodialysis.

TABLE 65. Presentation and Treatment of Alcohol Poisoning Alcohol Common Sources Major Findings Anion Gap Osmolar Gap Antidote Ethanol Alcoholic beverages CNS depression Possible Yes Supportive care Nausea, emesis lsopropyl Rubbing alcohol CNS depression No Yes Supportive care alcohol Disinfectants Ketone elevation Antifreeze Methanol Windshield wiperfluid CNS depression Yes Yes Fomepizole De-icing solutions Vision loss Ethanol (only if fomepizole is not available) Solvents Hypotension HD {or severe acidemia, very "Moonshine" large ingestions, severe CNS depression, and any visual impairment Ethylene Antifreeze CNS depression Yes Yes Fomepizole glycol De-icing solutions AKI Ethanol (only if fomepizole is not available) Solvents Hypocalcemia HD for severe acidemia, very Hypotension large ingestions, severe CNS depression, AKl, and systemic collapse AKI = acute kidney injury; CNS = central nervous system; HD = hemodialysis. (CNS) inhibitor, thus leading to CNS depression, including loss t(Iy Potltrs i of consciousness and suppression of respiratory drive at high . Ethylene glycol and methanol ingestion are associated doses, which can lead to respiratory failure or aspiration with an increased anion gap metabolic acidosis as well events. as an increased osmolal gap. Ethanol is the most commonly ingested alcohol and the most often encountered toxicity (Table 6S). Other alcohols . Management of ethylene glycol and methanol ingestion ingested include ethylene glycol (antifreeze), methanol includes competitive inhibition of alcohol dehydroge- (wood alcohol), and isopropyl alcohol (rubbing alcohol). nase with intravenous fomepizole.

(CNS) inhibitor, thus leading to CNS depression, including loss t(Iy Potltrs i of consciousness and suppression of respiratory drive at high . Ethylene glycol and methanol ingestion are associated doses, which can lead to respiratory failure or aspiration with an increased anion gap metabolic acidosis as well events. as an increased osmolal gap. Ethanol is the most commonly ingested alcohol and the most often encountered toxicity (Table 6S). Other alcohols . Management of ethylene glycol and methanol ingestion ingested include ethylene glycol (antifreeze), methanol includes competitive inhibition of alcohol dehydroge- (wood alcohol), and isopropyl alcohol (rubbing alcohol). nase with intravenous fomepizole. These all have CNS depressant effects similar to those of . Hemodialysis rapidly and effectively removes alcohols ethanol. However, after ingestion, ethylene glycol is metabo and should be performed as soon as possible in con- lized by alcohol dehydrogenase to oxalic acid, which crystal- firmed ethylene glycol or methanol poisoning or in sus- izes in the renal tubules and can lead to permanent kidney pected cases associated with high anion gap metabolic damage. Methanol is metabolized to formic acid, which is acidosis or symptoms of end organ damage. toxic to the retina and leads to blindness. When either of these alcohols has been ingested, there is an increased anion Carbon Monoxide Poisoning gap metabolic acidosis, as well as an increased osmolal gap Carbon monoxide (CO) is a colorless, odorless product of (see MKSAP 19 Nephrologr: Increased Anion Gap Metabolic hydrocarbon combustion that is readily absorbed into the cir- Acidosis). Management includes competitive inhibition culation when inhaled and binds avidly to hemoglobin to form of alcohol dehydrogenase with intravenous fomepizole. If carboxyhemoglobin, displacing oxygen and causing tissue fomepizole is not available, intravenous ethanol also com- hypoxia and ischemia. CO toxicity occurs almost exclusively in petes with other alcohols to reduce toxic metabolite forma enclosed areas where combustion is occurring and is often tion. Hemodialysis rapidly and effectively removes alcohols accidental, but it may be intentional in suicide attempts. and should be performed as soon as possible in confirmed Exposed patients present with headache, nausea, malaise, ethylene glycol or methanol poisoning or in suspected cases confusion, syncope, seizures, or coma. Patients with coronary associated with high anion gap metabolic acidosis or symp artery disease may develop signs and symptoms of cardiac toms of end organ damage (visual impairment or kidney ischemia. injury). Pulse oximetry is not helpful, as current transcutaneous Isopropyl alcohol has no toxic metabolites and does not oximetry technologz does not differentiate between oxyhemo elevate the anion gap, although it does increase the osmolal gap. globin and carboxyhemoglobin. Blood gas analysis, including Treatment for ethanol and isopropyl toxicity is supportive. CO oximetry will provide the carboxyhemoglobin level, which

These all have CNS depressant effects similar to those of . Hemodialysis rapidly and effectively removes alcohols ethanol. However, after ingestion, ethylene glycol is metabo and should be performed as soon as possible in con- lized by alcohol dehydrogenase to oxalic acid, which crystal- firmed ethylene glycol or methanol poisoning or in sus- izes in the renal tubules and can lead to permanent kidney pected cases associated with high anion gap metabolic damage. Methanol is metabolized to formic acid, which is acidosis or symptoms of end organ damage. toxic to the retina and leads to blindness. When either of these alcohols has been ingested, there is an increased anion Carbon Monoxide Poisoning gap metabolic acidosis, as well as an increased osmolal gap Carbon monoxide (CO) is a colorless, odorless product of (see MKSAP 19 Nephrologr: Increased Anion Gap Metabolic hydrocarbon combustion that is readily absorbed into the cir- Acidosis). Management includes competitive inhibition culation when inhaled and binds avidly to hemoglobin to form of alcohol dehydrogenase with intravenous fomepizole. If carboxyhemoglobin, displacing oxygen and causing tissue fomepizole is not available, intravenous ethanol also com- hypoxia and ischemia. CO toxicity occurs almost exclusively in petes with other alcohols to reduce toxic metabolite forma enclosed areas where combustion is occurring and is often tion. Hemodialysis rapidly and effectively removes alcohols accidental, but it may be intentional in suicide attempts. and should be performed as soon as possible in confirmed Exposed patients present with headache, nausea, malaise, ethylene glycol or methanol poisoning or in suspected cases confusion, syncope, seizures, or coma. Patients with coronary associated with high anion gap metabolic acidosis or symp artery disease may develop signs and symptoms of cardiac toms of end organ damage (visual impairment or kidney ischemia. injury). Pulse oximetry is not helpful, as current transcutaneous Isopropyl alcohol has no toxic metabolites and does not oximetry technologz does not differentiate between oxyhemo elevate the anion gap, although it does increase the osmolal gap. globin and carboxyhemoglobin. Blood gas analysis, including Treatment for ethanol and isopropyl toxicity is supportive. CO oximetry will provide the carboxyhemoglobin level, which 83

Specific Critical Care Topics is less than 3% in normal individuals. Smokers may have up to or competitive binding of the cyanide to remove it from the 10'1, to 15% carboxyhemoglobin; any,thing higher is consistent mitochondrial respiration system. Hydroxocobalamin avidly with CO poisoning. binds to cyanide to produce cyanocobalamin, which is solu- Because oxygen and CO competitively bind to hemo- ble, nontoxic, and readily excreted. The usual dose is 5 g for globin, the primary treatment is supplemental oxygen. Once an adult. Other antidotes include nitrites (amyl nitrite and the CO exposure has been stopped, the half life of carboxy sodium nitrite) to induce methemoglobin, which in turn hemoglobin is 300 minutes if patients are breathing ambient binds cyanide, as well as sodium thiosulfate, which donates air, 90 minutes if breathing 100'/" oxygen, and 30 minutes if sulfur to combine with cyanide, producing harmless thiocy given hyperbaric oxygen in a chamber where the pressure is anate. Inducing methemoglobinemia in inhalation injury gradually increased to 2 to 3 times the normal atmospheric victims who may also have high levels of carboxyhemoglobin pressure. Patients with high levels of carboxyhemoglobin (2s% is not safe, so nitrite therapy should be avoided. Of these and greater) and evidence of organ ischemia should be treated potential treatment strategies, hydroxocobalamin is the most with hyperbaric oxygen if possible. commonly recommended because of the ease and safefy of In addition to the immediate complications resulting administration. from tissue hypoxia in the setting of CO toxicity, there are also delayed neurologic sequelae in approximately 40% of severe TABLE 66. Toxic Syndromes and Their Manifestations cases of CO poisoning. The mechanism is poorly understood, Syrdrome Manifustations RepresentativeDrugs but probably relates to ischemic damage sustained in specific, Sympathomimetic Tachycardia Cocaine oxygen sensitive areas ofthe brain. These delayed neurocogni- Hypertension Amphetamines tive and personality defects usually appear within 20 days of Diaphoresis Ephedrine the exposure, but they can appear later and may last for a year Agitation Caffeine or longer. There is weak evidence that hyperbaric oxygen therapy reduces the risk and severity of these delayed neuro- Seizures

is less than 3% in normal individuals. Smokers may have up to or competitive binding of the cyanide to remove it from the 10'1, to 15% carboxyhemoglobin; any,thing higher is consistent mitochondrial respiration system. Hydroxocobalamin avidly with CO poisoning. binds to cyanide to produce cyanocobalamin, which is solu- Because oxygen and CO competitively bind to hemo- ble, nontoxic, and readily excreted. The usual dose is 5 g for globin, the primary treatment is supplemental oxygen. Once an adult. Other antidotes include nitrites (amyl nitrite and the CO exposure has been stopped, the half life of carboxy sodium nitrite) to induce methemoglobin, which in turn hemoglobin is 300 minutes if patients are breathing ambient binds cyanide, as well as sodium thiosulfate, which donates air, 90 minutes if breathing 100'/" oxygen, and 30 minutes if sulfur to combine with cyanide, producing harmless thiocy given hyperbaric oxygen in a chamber where the pressure is anate. Inducing methemoglobinemia in inhalation injury gradually increased to 2 to 3 times the normal atmospheric victims who may also have high levels of carboxyhemoglobin pressure. Patients with high levels of carboxyhemoglobin (2s% is not safe, so nitrite therapy should be avoided. Of these and greater) and evidence of organ ischemia should be treated potential treatment strategies, hydroxocobalamin is the most with hyperbaric oxygen if possible. commonly recommended because of the ease and safefy of In addition to the immediate complications resulting administration. from tissue hypoxia in the setting of CO toxicity, there are also delayed neurologic sequelae in approximately 40% of severe TABLE 66. Toxic Syndromes and Their Manifestations cases of CO poisoning. The mechanism is poorly understood, Syrdrome Manifustations RepresentativeDrugs but probably relates to ischemic damage sustained in specific, Sympathomimetic Tachycardia Cocaine oxygen sensitive areas ofthe brain. These delayed neurocogni- Hypertension Amphetamines tive and personality defects usually appear within 20 days of Diaphoresis Ephedrine the exposure, but they can appear later and may last for a year Agitation Caffeine or longer. There is weak evidence that hyperbaric oxygen therapy reduces the risk and severity of these delayed neuro- Seizures logic sequelae. Mydriasis Cholinergic "SLUDGE" Organophosphates f,EY POIT{TS (salivation, (insecticides, sarin) HVC . Pulse oximetry is not helpful in diagnosing carbon lacrimation, Carbamates increased monoxide poisoning, as it does not differentiate between urination and Physostigmine oxyhemoglobin and carboxyhemoglobin. defecation, gastrointesti nal Edrophonium o Patients with high levets of carboxyhemoglobin (25'L or upset, and Nicotine higher) and evidence oforgan dysfunction should be emesis) treated with hyperbaric oxygen if possible. Confusion Bronchorrhea Cyanide Poisoning Cyanide is one of the most lethal poisons known. It inhibits Bradycardia cellular respiration by binding to cytochrome oxidase o., in the Miosis mitochondria, blocking the cells' ability to use oxygen for Anticholinergic Hyperthermia Antihistamines aerobic metabolism. This results in clinical signs of hypoxia, Dry skin and Tricyclic despite normal oxyhemoglobin saturation. Symptoms olten mucous antidepressants include headache, anxiety, nausea, and either a metallic or bit- membranes Anti-Parkinson ter almond odor and taste. More severe or prolonged exposure Agitation, agents can lead to coma, seizures, liver or kidney injury vomiting, delirium Atropine ischemic pain, rhabdomyolysis, and death. Serum lactate Tachycardia, Scopolamine elevation is a sensitive but nonspecific marker for cyanide tachypnea

logic sequelae. Mydriasis Cholinergic "SLUDGE" Organophosphates f,EY POIT{TS (salivation, (insecticides, sarin) HVC . Pulse oximetry is not helpful in diagnosing carbon lacrimation, Carbamates increased monoxide poisoning, as it does not differentiate between urination and Physostigmine oxyhemoglobin and carboxyhemoglobin. defecation, gastrointesti nal Edrophonium o Patients with high levets of carboxyhemoglobin (25'L or upset, and Nicotine higher) and evidence oforgan dysfunction should be emesis) treated with hyperbaric oxygen if possible. Confusion Bronchorrhea Cyanide Poisoning Cyanide is one of the most lethal poisons known. It inhibits Bradycardia cellular respiration by binding to cytochrome oxidase o., in the Miosis mitochondria, blocking the cells' ability to use oxygen for Anticholinergic Hyperthermia Antihistamines aerobic metabolism. This results in clinical signs of hypoxia, Dry skin and Tricyclic despite normal oxyhemoglobin saturation. Symptoms olten mucous antidepressants include headache, anxiety, nausea, and either a metallic or bit- membranes Anti-Parkinson ter almond odor and taste. More severe or prolonged exposure Agitation, agents can lead to coma, seizures, liver or kidney injury vomiting, delirium Atropine ischemic pain, rhabdomyolysis, and death. Serum lactate Tachycardia, Scopolamine elevation is a sensitive but nonspecific marker for cyanide tachypnea toxicity. A normal lactate concentration effectively rules out Hypertension signifi cant cyanide exposure. Mydriasis Cyanide can be ingested or inhaled and is absorbed read Opioids Miosis Morphine, fentanyl, ily and acts quickly to inhibit cellular metabolism. Inhalation oxycodone and Respiratory exposure is common in house fires, where cyanide is produced related drugs depression and aerosolized when vinyl burns. Cyanide is a common coex- Heroin Lethargy, posure with CO. Prolonged nitroprusside infusion may also confusion result in cyanide toxicity. Hypothermia Successful treatment depends on early recognition of Bradycardia cyanide toxicity, elimination of ongoing exposure (e.g., Hypotension removal of contaminated clothing), and either neutralization

toxicity. A normal lactate concentration effectively rules out Hypertension signifi cant cyanide exposure. Mydriasis Cyanide can be ingested or inhaled and is absorbed read Opioids Miosis Morphine, fentanyl, ily and acts quickly to inhibit cellular metabolism. Inhalation oxycodone and Respiratory exposure is common in house fires, where cyanide is produced related drugs depression and aerosolized when vinyl burns. Cyanide is a common coex- Heroin Lethargy, posure with CO. Prolonged nitroprusside infusion may also confusion result in cyanide toxicity. Hypothermia Successful treatment depends on early recognition of Bradycardia cyanide toxicity, elimination of ongoing exposure (e.g., Hypotension removal of contaminated clothing), and either neutralization 84

Specific Critical Care Topics TEY POIlIT An early empiric trial of the opioid antagonist naloxone is o Successful treatment of cyanide poisoning depends on warranted when opioid overdose is suspected to reverse res- piratory depression and depressed mental stafus. When used, early recognition of cyanide toxicity, elimination of ongoing exposure, and administration of hydroxocobal- it should be titrated to adequate respiratory rate and not to mental status. It is important to remember that naloxone has a amin to remove the cyanide from the mitochondrial very short half-life, and its antidote effects will usually wear respiration system. off before the opioid effects are gone. Patients should be observed for signs of opioid withdrawal (which is not fatal and Toxicity of Drugs of Abuse requires only supportive care) and for continued or recurrent Drugs of abuse may be taken singly or in combination, and an signs of respiratory distress, which may require repeated dos- accurate history may be impossible to obtain as a result of ing of naloxone. alteration of mental status, reluctance on the part of the patient Administration of flumazenil for suspected benzodiaze- to disclose drug use, and insufficient or incorrect knowledge pine overdose is more problematic, as reversing the effect of about the composition of such drugs. Clinical toxic syndromes, benzodiazepines can lead to life-threatening CNS activation, or constellations of symptoms and signs indicative of certain including seizures, which are most likely in patients receiving classes of drugs, can be recognized and provide clues as to benzodiazepines chronically. It is usually best to manage what should be done for effective medical management of patients with ventilator support and allow elimination of the overdose (Table 66 and Table 67). agent over time. ln addition to seeking to identify the specific agents or In patients who have received sympathomimetic classes ol drugs taken, care of overdose patients is primarily agents, such as cocaine or amphetamines, benzodiazepines supportive; maintenance of airway patency and ventilation is are the cornerstone oftherapy for agitation. B Blocker med critically important in patients with decreased mental status. ications should be avoided, as they will block the beta- Patients may need intubation to protect the ainvay from aspi adrenergic receptors and, at least theoretically, leave the ration or in cases of respiratory failure where respiratory drive activated alpha receptors unopposed, thus leading to severe is impaired by drugs. hypertension.

TEY POIlIT An early empiric trial of the opioid antagonist naloxone is o Successful treatment of cyanide poisoning depends on warranted when opioid overdose is suspected to reverse res- piratory depression and depressed mental stafus. When used, early recognition of cyanide toxicity, elimination of ongoing exposure, and administration of hydroxocobal- it should be titrated to adequate respiratory rate and not to mental status. It is important to remember that naloxone has a amin to remove the cyanide from the mitochondrial very short half-life, and its antidote effects will usually wear respiration system. off before the opioid effects are gone. Patients should be observed for signs of opioid withdrawal (which is not fatal and Toxicity of Drugs of Abuse requires only supportive care) and for continued or recurrent Drugs of abuse may be taken singly or in combination, and an signs of respiratory distress, which may require repeated dos- accurate history may be impossible to obtain as a result of ing of naloxone. alteration of mental status, reluctance on the part of the patient Administration of flumazenil for suspected benzodiaze- to disclose drug use, and insufficient or incorrect knowledge pine overdose is more problematic, as reversing the effect of about the composition of such drugs. Clinical toxic syndromes, benzodiazepines can lead to life-threatening CNS activation, or constellations of symptoms and signs indicative of certain including seizures, which are most likely in patients receiving classes of drugs, can be recognized and provide clues as to benzodiazepines chronically. It is usually best to manage what should be done for effective medical management of patients with ventilator support and allow elimination of the overdose (Table 66 and Table 67). agent over time. ln addition to seeking to identify the specific agents or In patients who have received sympathomimetic classes ol drugs taken, care of overdose patients is primarily agents, such as cocaine or amphetamines, benzodiazepines supportive; maintenance of airway patency and ventilation is are the cornerstone oftherapy for agitation. B Blocker med critically important in patients with decreased mental status. ications should be avoided, as they will block the beta- Patients may need intubation to protect the ainvay from aspi adrenergic receptors and, at least theoretically, leave the ration or in cases of respiratory failure where respiratory drive activated alpha receptors unopposed, thus leading to severe is impaired by drugs. hypertension. TABTE 67. Presentation and Management of Some Drugs of Abuse Drug Class Examples Examination Findings Antidote Opioids Heroin, oxycodone, J HR, J temp, J BB J RR, miosis Naloxone fentanyl analogs Benzod iazepines Lorazepam CNS depression, usually normalvital signs Flumazenil (not generally and eye examination recommended; may be complicated by seizure) Sympathomimetics All t HR, t BB 1temp, diaphoresis, mydriasis, Benzodiazepines are first-line for agitation, seizure, 1CK, t liver chemistry agitation; avoid B-blockers for studies, 1Cr hypertension; haloperidol may Specific drugs: worsen hyperthermia Cocaine Myocardial infarction prominent; 30-minute duration Methamphetamine Violent agitation prominent; J Na; 20-hour duration M DMA ("ecstasy") J Na, serotonin syndrome Bath salts ("plant food") Hallucinations, violent agitation common; duration up to 48 hours; negative urine drug screen Hallucinogens Dextro methorp ha n 1 HR, 1 BP, agitation, coma

TABTE 67. Presentation and Management of Some Drugs of Abuse Drug Class Examples Examination Findings Antidote Opioids Heroin, oxycodone, J HR, J temp, J BB J RR, miosis Naloxone fentanyl analogs Benzod iazepines Lorazepam CNS depression, usually normalvital signs Flumazenil (not generally and eye examination recommended; may be complicated by seizure) Sympathomimetics All t HR, t BB 1temp, diaphoresis, mydriasis, Benzodiazepines are first-line for agitation, seizure, 1CK, t liver chemistry agitation; avoid B-blockers for studies, 1Cr hypertension; haloperidol may Specific drugs: worsen hyperthermia Cocaine Myocardial infarction prominent; 30-minute duration Methamphetamine Violent agitation prominent; J Na; 20-hour duration M DMA ("ecstasy") J Na, serotonin syndrome Bath salts ("plant food") Hallucinations, violent agitation common; duration up to 48 hours; negative urine drug screen Hallucinogens Dextro methorp ha n 1 HR, 1 BP, agitation, coma Lysergic acid Mild 1 HR; 1 BP; rare l temp and Benzodiazepines are {irst-line for diethylamide (LSD) hemodynamic instability agitation Haloperidol is second-line Phencyclidine (PCP) Variable mental status: l agitation, CNS depression, nystagmus Synthetic ca n nabinoids 1 HR; greater agitation than with marijuana [ 5prce, r.-z ) l Cr; negative urine drug screen BP = b ood pressure; CK= creatine kinase; CNS = central nervous system; Cr = creat nine; HR = heart rate; MDMA= 3-4 methylenedioxymethamphetamine; Na = sodium; RR = respiration rate; temp = temperature.

Lysergic acid Mild 1 HR; 1 BP; rare l temp and Benzodiazepines are {irst-line for diethylamide (LSD) hemodynamic instability agitation Haloperidol is second-line Phencyclidine (PCP) Variable mental status: l agitation, CNS depression, nystagmus Synthetic ca n nabinoids 1 HR; greater agitation than with marijuana [ 5prce, r.-z ) l Cr; negative urine drug screen BP = b ood pressure; CK= creatine kinase; CNS = central nervous system; Cr = creat nine; HR = heart rate; MDMA= 3-4 methylenedioxymethamphetamine; Na = sodium; RR = respiration rate; temp = temperature. 85

Specific Critical Care Topics Hallucinogenic agents have no antidote, so care is their airway, administration of activated charcoal may be supportive, including maintaining the airway, ventilation, beneficial if it can be given within 1 to 2 hours of ingestion. and hemodynamic support. These patients may be extremely Acetaminophen overdose is discussed in MKSAP 19 agitated and combative, requiring physical restraints or Gastroenterology and Hepatology, and salicylate overdose sedation to prevent them from harming themselves and in MKSAP 19 Nephrology. others. Overdose of Therapeutic Drugs Acute Abdominal Surgical Patients may overdose on prescribed medications either Emergencies inadvertently or intentionally, and often many medications A large number of conditions can cause abdominal pain, dis- are taken together, sometimes with alcohol. Information tention, and rigidity. Although many of them can and should about suicidal ideation or intent, what medications a be managed medically, some require surgery and timely diag patient and family members have been prescribed, what nosis followed by surgical intervention is needed to improve prescriptions were filled, events reported by the patient or survival. Imaging decisions should be based on history and bystanders, and clinical signs and symptoms are all impor- examination findings, and they should not delay intervention tant in determining the nature of an overdose (Table 68). (Table 69). For further discussion of abdominal compartment If patients are alert and cooperative enough to protect syndrome see MKSAP 19 Nephrologz.

Overdose of Therapeutic Drugs Acute Abdominal Surgical Patients may overdose on prescribed medications either Emergencies inadvertently or intentionally, and often many medications A large number of conditions can cause abdominal pain, dis- are taken together, sometimes with alcohol. Information tention, and rigidity. Although many of them can and should about suicidal ideation or intent, what medications a be managed medically, some require surgery and timely diag patient and family members have been prescribed, what nosis followed by surgical intervention is needed to improve prescriptions were filled, events reported by the patient or survival. Imaging decisions should be based on history and bystanders, and clinical signs and symptoms are all impor- examination findings, and they should not delay intervention tant in determining the nature of an overdose (Table 68). (Table 69). For further discussion of abdominal compartment If patients are alert and cooperative enough to protect syndrome see MKSAP 19 Nephrologz. Medication Key Clinical Findings Treatment Notes Nonopioid analgesics Acetaminophen t liver chemistry studies, 'l Cr, N-acetylcysteine Transfer to liver transplant center if 1 lNR, encephalopathy, cerebral severe edema, vomiting Salicylates Mixed respiratory alkalosis/anion Forced diuresis, bicarbonate Target urine pH 7.5-8.0; hemodialysis gap metabolic acidosis, tinnitus, infusion, glucose if acute kidney injury or severe agitation, confusion, hyperthermia toxicity Cardiovascular

Medication Key Clinical Findings Treatment Notes Nonopioid analgesics Acetaminophen t liver chemistry studies, 'l Cr, N-acetylcysteine Transfer to liver transplant center if 1 lNR, encephalopathy, cerebral severe edema, vomiting Salicylates Mixed respiratory alkalosis/anion Forced diuresis, bicarbonate Target urine pH 7.5-8.0; hemodialysis gap metabolic acidosis, tinnitus, infusion, glucose if acute kidney injury or severe agitation, confusion, hyperthermia toxicity Cardiovascular B-Blocker, calcium J HR, J Be heart block; altered Atropine 1 mg lV up to 3 doses, Treatments may be added channel blocker mental status if p-blocker glucagon, calcium chloride, sequentially or initiated vasopressors, cardiac pacemaker simultaneously depending on (if indicated), high-dose insulin severity of case and response to and glucose, lV lipid emulsion treatment Digoxin J HR, arrhythmia, nausea, emesis, Digoxin-specific antibody Use of antibody lowers K*; abdominal pain, confusion, hemodialysis not effective weakness Anticholinergics Tricyclic J BP, sedation, seizure, Bicarbonate infusion titrated to Physosti g m i ne contraindicated antidepressants anticholinergic signs, prolonged ORS duration; benzodiazepines ORS, arrhythmia for seizure Antihistamines Anticholinergic signs, including Benzodiazepines; physostigmine Physostigmine use requires agitation and seizures if isolated anticholinergic continuous cardiac monitor and overdose bedside atropine Hypoglycemic Sulfonylurea J glucose, confusion, seizure, lV glucose + octreotide, glucagon Monitor for J glucose for 48 hours anxiety, diaphoresis, tremor lM =temporizing if large ingestion Metformin t lactate, abdominal pain Hemodialysis for severe J pH or Glucose usually normal if isolated acute kidney injury metformin ingestion Others Lithium Gl distress, confusion, ataxia, Hemodialysis if lithium level Serum level can guide need for tremor, myoclonic jerks, diabetes >4 mEq/L (4 mmol/L) or severe hemodialysis, confirm diagnosis insipidus symptoms SSRI/SNRI Agitation, myoclonus, t reflexes, Benzodiazepines, cyproheptadine Venlafaxine has t cardiac toxicity rigidity, fever, t HR if severe

B-Blocker, calcium J HR, J Be heart block; altered Atropine 1 mg lV up to 3 doses, Treatments may be added channel blocker mental status if p-blocker glucagon, calcium chloride, sequentially or initiated vasopressors, cardiac pacemaker simultaneously depending on (if indicated), high-dose insulin severity of case and response to and glucose, lV lipid emulsion treatment Digoxin J HR, arrhythmia, nausea, emesis, Digoxin-specific antibody Use of antibody lowers K*; abdominal pain, confusion, hemodialysis not effective weakness Anticholinergics Tricyclic J BP, sedation, seizure, Bicarbonate infusion titrated to Physosti g m i ne contraindicated antidepressants anticholinergic signs, prolonged ORS duration; benzodiazepines ORS, arrhythmia for seizure Antihistamines Anticholinergic signs, including Benzodiazepines; physostigmine Physostigmine use requires agitation and seizures if isolated anticholinergic continuous cardiac monitor and overdose bedside atropine Hypoglycemic Sulfonylurea J glucose, confusion, seizure, lV glucose + octreotide, glucagon Monitor for J glucose for 48 hours anxiety, diaphoresis, tremor lM =temporizing if large ingestion Metformin t lactate, abdominal pain Hemodialysis for severe J pH or Glucose usually normal if isolated acute kidney injury metformin ingestion Others Lithium Gl distress, confusion, ataxia, Hemodialysis if lithium level Serum level can guide need for tremor, myoclonic jerks, diabetes >4 mEq/L (4 mmol/L) or severe hemodialysis, confirm diagnosis insipidus symptoms SSRI/SNRI Agitation, myoclonus, t reflexes, Benzodiazepines, cyproheptadine Venlafaxine has t cardiac toxicity rigidity, fever, t HR if severe SSRI = selective serotonin reuptake inhibitor.

B-Blocker, calcium J HR, J Be heart block; altered Atropine 1 mg lV up to 3 doses, Treatments may be added channel blocker mental status if p-blocker glucagon, calcium chloride, sequentially or initiated vasopressors, cardiac pacemaker simultaneously depending on (if indicated), high-dose insulin severity of case and response to and glucose, lV lipid emulsion treatment Digoxin J HR, arrhythmia, nausea, emesis, Digoxin-specific antibody Use of antibody lowers K*; abdominal pain, confusion, hemodialysis not effective weakness Anticholinergics Tricyclic J BP, sedation, seizure, Bicarbonate infusion titrated to Physosti g m i ne contraindicated antidepressants anticholinergic signs, prolonged ORS duration; benzodiazepines ORS, arrhythmia for seizure Antihistamines Anticholinergic signs, including Benzodiazepines; physostigmine Physostigmine use requires agitation and seizures if isolated anticholinergic continuous cardiac monitor and overdose bedside atropine Hypoglycemic Sulfonylurea J glucose, confusion, seizure, lV glucose + octreotide, glucagon Monitor for J glucose for 48 hours anxiety, diaphoresis, tremor lM =temporizing if large ingestion Metformin t lactate, abdominal pain Hemodialysis for severe J pH or Glucose usually normal if isolated acute kidney injury metformin ingestion Others Lithium Gl distress, confusion, ataxia, Hemodialysis if lithium level Serum level can guide need for tremor, myoclonic jerks, diabetes >4 mEq/L (4 mmol/L) or severe hemodialysis, confirm diagnosis insipidus symptoms SSRI/SNRI Agitation, myoclonus, t reflexes, Benzodiazepines, cyproheptadine Venlafaxine has t cardiac toxicity rigidity, fever, t HR if severe SSRI = selective serotonin reuptake inhibitor. 86

Specific Critical Care Topics a TABLE 69, Acute Abdominal Emergencies Diagnosis Presentation Diagnostic lmaging Notes Acute cholecystitis Persistent peritoneal RUQ or Ultrasonography 1 alkaline phosphatase, t bilirubin and cholangitis epigastric pain, fever, emesis, suggests cholangitis but typically positive Murphy sign EUS and ERCP for diagnosis and not cholecystitis treatment of cholangitis Bowel obstruction Cramping pain, emesis, distention, Radiography: dilated loops of Top causes: incarcerated hernia, obstipation, dehyd ration bowel with air-fluid levels adhesions, volvulus, intussusception CT: identifies cause, complications Acute appendicitis Classic: periumbilical then RLO Often unnecessary Pain quality and location vary with pain, emesis, 1 leukocyte count appendix location CT or ultrasonography if unclear Peptic ulcer Abrupt peritoneal pain, later Radiography: free air Surgery necessary in majority of perforation distention and hypovolemia CASES CT if unclear r Acute mesenteric Pain out of proportion to CT angiography or conventional l amylase, t phosphate common ischemia examination findings, vomiting, arteriography hypotension, risk factors for Regular CT and lactate can be thrombosis, embolism normal early in course ,

TABLE 69, Acute Abdominal Emergencies Diagnosis Presentation Diagnostic lmaging Notes Acute cholecystitis Persistent peritoneal RUQ or Ultrasonography 1 alkaline phosphatase, t bilirubin and cholangitis epigastric pain, fever, emesis, suggests cholangitis but typically positive Murphy sign EUS and ERCP for diagnosis and not cholecystitis treatment of cholangitis Bowel obstruction Cramping pain, emesis, distention, Radiography: dilated loops of Top causes: incarcerated hernia, obstipation, dehyd ration bowel with air-fluid levels adhesions, volvulus, intussusception CT: identifies cause, complications Acute appendicitis Classic: periumbilical then RLO Often unnecessary Pain quality and location vary with pain, emesis, 1 leukocyte count appendix location CT or ultrasonography if unclear Peptic ulcer Abrupt peritoneal pain, later Radiography: free air Surgery necessary in majority of perforation distention and hypovolemia CASES CT if unclear r Acute mesenteric Pain out of proportion to CT angiography or conventional l amylase, t phosphate common ischemia examination findings, vomiting, arteriography hypotension, risk factors for Regular CT and lactate can be thrombosis, embolism normal early in course , s Toxic megacolon Pain, diarrhea, fever, 1 HR, J BB Radiography: dilated colon, Causes: inflammatory bowel i confusion air-fluid levels in colon disease, Clostridioides difficile infection l CT if unclear ]

s Toxic megacolon Pain, diarrhea, fever, 1 HR, J BB Radiography: dilated colon, Causes: inflammatory bowel i confusion air-fluid levels in colon disease, Clostridioides difficile infection l CT if unclear ] Ruptured J BB abdominal and/or flank pain, Unnecessary if high suspicion and Risk {actors: older age, male, abdominal aortic pulsatile mass unstable smoking, hypertension, family aneurysm history of aneurysm CT or ultrasonography if unclear i Ectopic pregnancy J BB J Hb,'l hCG, abdominal pain, Transvaginal ultrasonography High mortality without early surgery with tubal rupture vaginal bleeding BP = blood pressure; ERCP = endoscopic retrograde cholangiopancreatography; EUS = endoscopic ultrasonography; Hb = hemoglobin; hCG = human chorionic gonadotropin; HR = heart rate; RLO = right lower quadrant; RUQ = right upper quadrant; temp = temperature. I I

Ruptured J BB abdominal and/or flank pain, Unnecessary if high suspicion and Risk {actors: older age, male, abdominal aortic pulsatile mass unstable smoking, hypertension, family aneurysm history of aneurysm CT or ultrasonography if unclear i Ectopic pregnancy J BB J Hb,'l hCG, abdominal pain, Transvaginal ultrasonography High mortality without early surgery with tubal rupture vaginal bleeding BP = blood pressure; ERCP = endoscopic retrograde cholangiopancreatography; EUS = endoscopic ultrasonography; Hb = hemoglobin; hCG = human chorionic gonadotropin; HR = heart rate; RLO = right lower quadrant; RUQ = right upper quadrant; temp = temperature. I I i Fat Embolism The most frequent critical care emergencies in pregnancy t are summarized in Table 70. Fat embolism is the entrance of flat globules in the systemic \ circulation. It is a relatively common occurrence after trauma I involving long bone fractures. Fat embolism syndrome, how- L ever, is a rare but potentially Iethal complication resulting Encephalopathy t from systemic manifestations of fat emboli when they lodge in Alterations in mental status are common in the ICU because of capillaries and arterioles. It is a clinical diagnosis centered on both critical illness and the ICU environment, which is disrup- t I the presence ofa triad ofrespiratory insufficiency, neurologic tive to sleep and inhibits contextual clues for orientation to I

i Fat Embolism The most frequent critical care emergencies in pregnancy t are summarized in Table 70. Fat embolism is the entrance of flat globules in the systemic \ circulation. It is a relatively common occurrence after trauma I involving long bone fractures. Fat embolism syndrome, how- L ever, is a rare but potentially Iethal complication resulting Encephalopathy t from systemic manifestations of fat emboli when they lodge in Alterations in mental status are common in the ICU because of capillaries and arterioles. It is a clinical diagnosis centered on both critical illness and the ICU environment, which is disrup- t I the presence ofa triad ofrespiratory insufficiency, neurologic tive to sleep and inhibits contextual clues for orientation to I \ dysfunction, and petechial rash in the appropriate clinical set time, place, and events. Many conditions involve mental status ting. High resolution CT findings are nonspecific, and imaging change, but three are most important in the context of critical t may be normal. There is no definitive therapy for established care medicine: delirium (addressed in Principles of Critical ! fat embolism syndrome. Treatment is supportive, and most Care), coma, and anoxic brain injury. L i patients recover spontaneously and completely, although mor tality can be as high as 5'2, to 20'2,. 1 Coma j Coma describes a condition of absent cortical function of I the CNS with intact brainstem function, whether a result of I

\ dysfunction, and petechial rash in the appropriate clinical set time, place, and events. Many conditions involve mental status ting. High resolution CT findings are nonspecific, and imaging change, but three are most important in the context of critical t may be normal. There is no definitive therapy for established care medicine: delirium (addressed in Principles of Critical ! fat embolism syndrome. Treatment is supportive, and most Care), coma, and anoxic brain injury. L i patients recover spontaneously and completely, although mor tality can be as high as 5'2, to 20'2,. 1 Coma j Coma describes a condition of absent cortical function of I the CNS with intact brainstem function, whether a result of I L Approach to the Critically lll illness, trauma, or medication. Patients in a coma do not Patient Who ls Pregnant respond to external stimuli. The Glasgow Coma Scale is an t The physiologic changes in pregnancy present a unique chal- instrument for assessing the severity of deficit based on i lenge to the management of these patients in the critical care three categories of stimulus response: eye response, verbal setting. Optimization of maternal physiologr without compro response, and motor response (Table 71). A Glasgow Coma L mising the well being of the fetus requires a multidisciplinary Scale score of 15 means a normal, alert (or fully arousable) l

L Approach to the Critically lll illness, trauma, or medication. Patients in a coma do not Patient Who ls Pregnant respond to external stimuli. The Glasgow Coma Scale is an t The physiologic changes in pregnancy present a unique chal- instrument for assessing the severity of deficit based on i lenge to the management of these patients in the critical care three categories of stimulus response: eye response, verbal setting. Optimization of maternal physiologr without compro response, and motor response (Table 71). A Glasgow Coma L mising the well being of the fetus requires a multidisciplinary Scale score of 15 means a normal, alert (or fully arousable) l L approach involving an intensivist, an obstetrician gznecologist, patient, and a score of 3 means no response at all. Physical I and a neonatologist. Particular attention must be given to the examination findings of brainstem (pupil or eye movement) I pharmacologz of medications, including the potential for fetal or motor (posturing) abnormalities might help localize i exposure from transfer across the placenta. disease in the CNS. In addition to a clinical examination, I t 87 I

Specific Critical Care Topics TABLE 70. Obstetric Critical Care Emergencies Presentation Causes Diagnosis Key Treatment Principles Dyspnea Status asthmaticus Diagnosis based on clinical lnhaled glucocorticoids presentation (preferentially budesonide or fluticasone); short-acting B2 agonists and short courses of systemic glucocorticoids can be used. lntubation and mechanical ventilation if needed Venous thromboembolism Ultrasonography if DW suspected, Low-molecular-weight-heparin therapy ventilation/perfusion scan, CT recommended pulmonary angiography Pneumonia Chest radiography Avoid fluoroquinolones and tetracyclines Treat exposure to influenza with oseltamivir

Pneumonia Chest radiography Avoid fluoroquinolones and tetracyclines Treat exposure to influenza with oseltamivir Pulmonary edema; specific Chest radiography, Furosemide obstetric etiologies: preeclampsia, echocardiogram, invasive Nitroglycerine, hydralazine or calcium tocolytic therapy, peripartum hemodynamic monitoring if channel blockers for preload/afterload cardiomyopathy needed reduction

Pulmonary edema; specific Chest radiography, Furosemide obstetric etiologies: preeclampsia, echocardiogram, invasive Nitroglycerine, hydralazine or calcium tocolytic therapy, peripartum hemodynamic monitoring if channel blockers for preload/afterload cardiomyopathy needed reduction ARDS; specific obstetric etiologies lntubation and mechanical ventilation to consider: amniotic fluid if needed embolism, acute fatty liver of Evaluation for delivery pregnancy, intrauterine infections No controlled data on safety of permissive hypercapnia, fluid- restrictive strategy, or prone positioning in pregnancy Hemorrhage Antepartum etiologies: abru ptio Abruptio placentae: clinical Resuscitation with fluids and blood placentae, placenta previa, uterine diagnosis (abrupt vaginal bleeding, products rupture back pain, contractions) Correct coagulopathy Postpartum hemorrhage: uterine Placenta previa diagnosed with Consideration to delivery atony, retained placenta u ltrasonog ra phy (tra nsa bdom ina l/ transvaginal ) Refractory bleeding : embolization/ surgical exploration Uterine rupture: clinical diagnosis (vaginal bleeding, abdominal pain, Hysterectomy shock, fetal compromise typically during labor) Hypertension Preeclampsia (hypertension with Clinical diagnosis; severe cases with Consideration to delivery proteinuria after 20 weeks' evidence of end-organ dysfunction gestation) Magnesium sulfate (to prevent eclampsia) Antihypertensives (labetalol, hydralazine, nifedipine) Seizure Eclampsia Clinical diagnosis: new-onset Maternal hemodynamic and seizures in a patient with respiratory support preeclampsia Magnesium sulfate Anti hypertensives (labetalol, hydralazine, nicardipine) Delivery ARDS = acute respiratory distress syndrome; DW = deep venous thrombosis.

ARDS; specific obstetric etiologies lntubation and mechanical ventilation to consider: amniotic fluid if needed embolism, acute fatty liver of Evaluation for delivery pregnancy, intrauterine infections No controlled data on safety of permissive hypercapnia, fluid- restrictive strategy, or prone positioning in pregnancy Hemorrhage Antepartum etiologies: abru ptio Abruptio placentae: clinical Resuscitation with fluids and blood placentae, placenta previa, uterine diagnosis (abrupt vaginal bleeding, products rupture back pain, contractions) Correct coagulopathy Postpartum hemorrhage: uterine Placenta previa diagnosed with Consideration to delivery atony, retained placenta u ltrasonog ra phy (tra nsa bdom ina l/ transvaginal ) Refractory bleeding : embolization/ surgical exploration Uterine rupture: clinical diagnosis (vaginal bleeding, abdominal pain, Hysterectomy shock, fetal compromise typically during labor) Hypertension Preeclampsia (hypertension with Clinical diagnosis; severe cases with Consideration to delivery proteinuria after 20 weeks' evidence of end-organ dysfunction gestation) Magnesium sulfate (to prevent eclampsia) Antihypertensives (labetalol, hydralazine, nifedipine) Seizure Eclampsia Clinical diagnosis: new-onset Maternal hemodynamic and seizures in a patient with respiratory support preeclampsia Magnesium sulfate Anti hypertensives (labetalol, hydralazine, nicardipine) Delivery ARDS = acute respiratory distress syndrome; DW = deep venous thrombosis. lumbar puncture and CNS imaging with MRI or CT scan are Anoxic Brain lnjury useful in diagnosing the cause of coma. Treatment is sup Anoxic brain injury refers to damage to the CNS caused by portive with efforts to reverse the specific cause of the coma prolonged, profound tissue hypoxia. There are many possible if possible. causes of such hypoxia, including near drowning, seizures,

lumbar puncture and CNS imaging with MRI or CT scan are Anoxic Brain lnjury useful in diagnosing the cause of coma. Treatment is sup Anoxic brain injury refers to damage to the CNS caused by portive with efforts to reverse the specific cause of the coma prolonged, profound tissue hypoxia. There are many possible if possible. causes of such hypoxia, including near drowning, seizures, 88 I

Bibliography TABLE 71 . Glasgow Coma Scale Response Score Eyes Does not open eyes 1 Opens eyes in response to painfulstimuli(when given pain) 2 Opens eyes in response to voice 3 Opens eyes spontaneously 4 Verbal Makes no sound lncomprehensible sounds (mumbles) 2 Utters inappropriate words 3 Confused, disorientated 4 Oriented, chats normally 5 Motor (physical reflexes) Makes no movements 1 Extension (straightens limb when given painful stimulus) 2 Abnormal flexion (flexes limbs indiscriminately when given painful stimulus) 3 Flexion/withdrawalto painfulstimuli(moves away when given painful stimulus) 4 Localizes painful stimuli (can pinpoint where pain is) 5

Abnormal flexion (flexes limbs indiscriminately when given painful stimulus) 3 Flexion/withdrawalto painfulstimuli(moves away when given painful stimulus) 4 Localizes painful stimuli (can pinpoint where pain is) 5 Obeys commands 6 Brain lnjury Classification Based on Score Total Score (Eyes + Verbal + Motor) Coma 3-8 Moderate brain injury 9-12 Mild brain injury 13-15

Obeys commands 6 Brain lnjury Classification Based on Score Total Score (Eyes + Verbal + Motor) Coma 3-8 Moderate brain injury 9-12 Mild brain injury 13-15 obstructed airway, lung disease, cardiac arrest, asphlxiation, Dempsey TM, Scanlon PD. Pulmonary function tests for the generalist: A brief review. Mayo CIin Proc. 201893163-771. [PMID: 29866281] doi:10.1016/j. and other inhalational injury. Brain imaging shows edema and mayocp.2018.04.009 loss of grey-white matter demarcation. Electroencephalographic Little BP Approach to chest computed tomography. Clin Chest Med. 2015;36: 727 -45, vli. [PMID: 260245961 doi:10.1016/j.ccm.2015.02.001 monitoring shows various patterns, from diffuse slowing (typ- Rambhia SH, D'Agostino CA, Noor A, et al. Thoracic ultrasound: technique, ical of many types of encephalopathy) to burst suppression or applications, and interpretation. Curr Probl Diagn Radiol. 2017 Jul Aug; seizure activity (indicative of more severe injury) to absence of 46:305 316. IPMID: 28185691] doi:10.1067/j.cpradiol.2016.12.003 brain electrical activity (which can indicate brain death). Singh SJ, Puhan MA, Andrianopoulos V, et al. An official systematic review of the European Respiratory Society/American Thoracic Society: measure Prognosis is often not immediately apparent, and patients ment properties of field walking tests in chronic respiratory disease with anoxic brain injury require supportive care for 3 to 5 days lEditorial]. Eur Respir 1.2014.44:1447 78. [PMID: 25359356] doi:10.1183/ o9031 936.OOl 50414 or longer before the extent of injury can be understood well Wang Z, Pianosi P! Keogh KA, et al. The diagnostic accuracy of fractional enough to be declared irreversible. exhaled nitric oxide testing in asthma; A systematic review and meta analyses. Mayo Clin Proc. 2018;93:i91 198. [PMID: 292750311 doi:i0.1016/j. XEY POITI mayocp.20U.11.012 . Prognosis for patients with anoxic brain injury is often Airways Disease not immediately apparent, and patients require sup- Beasley R, Holliday M, Reddel HK, et al; Novel START Study Team. Controlled portive care for 3 to 5 days or longer before the extent of trial of budesonide formoterol as needed for mild asthma. N Engl J Med. 2019:380:2020-2030. IPMID: 31112386] doi:10.1056/NEJMoa19O1963 injury can be understood well enough to be declared Cloutier MM, Dixon AE, Krishnan JA, et al. Managing asthma in adolescents irreversible. and adults, 2o2o asthma guideline update from the National Asthma Education and Prevention Program. jAMA. 2020;324:2301 2317. [PMID: 332700951 doi:10.1001/jama.2020.21974

obstructed airway, lung disease, cardiac arrest, asphlxiation, Dempsey TM, Scanlon PD. Pulmonary function tests for the generalist: A brief review. Mayo CIin Proc. 201893163-771. [PMID: 29866281] doi:10.1016/j. and other inhalational injury. Brain imaging shows edema and mayocp.2018.04.009 loss of grey-white matter demarcation. Electroencephalographic Little BP Approach to chest computed tomography. Clin Chest Med. 2015;36: 727 -45, vli. [PMID: 260245961 doi:10.1016/j.ccm.2015.02.001 monitoring shows various patterns, from diffuse slowing (typ- Rambhia SH, D'Agostino CA, Noor A, et al. Thoracic ultrasound: technique, ical of many types of encephalopathy) to burst suppression or applications, and interpretation. Curr Probl Diagn Radiol. 2017 Jul Aug; seizure activity (indicative of more severe injury) to absence of 46:305 316. IPMID: 28185691] doi:10.1067/j.cpradiol.2016.12.003 brain electrical activity (which can indicate brain death). Singh SJ, Puhan MA, Andrianopoulos V, et al. An official systematic review of the European Respiratory Society/American Thoracic Society: measure Prognosis is often not immediately apparent, and patients ment properties of field walking tests in chronic respiratory disease with anoxic brain injury require supportive care for 3 to 5 days lEditorial]. Eur Respir 1.2014.44:1447 78. [PMID: 25359356] doi:10.1183/ o9031 936.OOl 50414 or longer before the extent of injury can be understood well Wang Z, Pianosi P! Keogh KA, et al. The diagnostic accuracy of fractional enough to be declared irreversible. exhaled nitric oxide testing in asthma; A systematic review and meta analyses. Mayo Clin Proc. 2018;93:i91 198. [PMID: 292750311 doi:i0.1016/j. XEY POITI mayocp.20U.11.012 . Prognosis for patients with anoxic brain injury is often Airways Disease not immediately apparent, and patients require sup- Beasley R, Holliday M, Reddel HK, et al; Novel START Study Team. Controlled portive care for 3 to 5 days or longer before the extent of trial of budesonide formoterol as needed for mild asthma. N Engl J Med. 2019:380:2020-2030. IPMID: 31112386] doi:10.1056/NEJMoa19O1963 injury can be understood well enough to be declared Cloutier MM, Dixon AE, Krishnan JA, et al. Managing asthma in adolescents irreversible. and adults, 2o2o asthma guideline update from the National Asthma Education and Prevention Program. jAMA. 2020;324:2301 2317. [PMID: 332700951 doi:10.1001/jama.2020.21974 Bibliography Global Initiative for Asthma. Global stratery for asthma management and prevention, 2021. Accessed May 5, 2021. https://ginasthma.orglgina- Pulmonary Diagnostic Tests reports/ Counts SJ, Kim AW. Diagnostic imaging and newer modalities for thoracic Global Initiative for Chronic Obstructive Lung Disease. Global strateS/ for the diseases: PET/Computed tomographic imaging and endobronchial ultra- diagnosis, management, and prevention of chronic obstructive pulmonary sound for staging and its implication for lung cancer. Surg Clin North Am. disease: 2020 report. Accessed September 27, 2020. https://goldcopd.org/ 2077 ;97 :733-750. [PMID: 28728712] doi:10.1016/j.suc. 2Ol7.O3.Ol2 gold reports/

Bibliography Global Initiative for Asthma. Global stratery for asthma management and prevention, 2021. Accessed May 5, 2021. https://ginasthma.orglgina- Pulmonary Diagnostic Tests reports/ Counts SJ, Kim AW. Diagnostic imaging and newer modalities for thoracic Global Initiative for Chronic Obstructive Lung Disease. Global strateS/ for the diseases: PET/Computed tomographic imaging and endobronchial ultra- diagnosis, management, and prevention of chronic obstructive pulmonary sound for staging and its implication for lung cancer. Surg Clin North Am. disease: 2020 report. Accessed September 27, 2020. https://goldcopd.org/ 2077 ;97 :733-750. [PMID: 28728712] doi:10.1016/j.suc. 2Ol7.O3.Ol2 gold reports/ 89