**3.3 Malignant hyperthermia (MH)**

MH is a genetic disorder which results in a hypermetabolic response to volatile anesthetics and depolarizing muscle relaxants [48]. This pathologic response to these medications results from caused the release of excessive calcium from the sarcoplasmic reticulum, which leads to uncoupling of oxidative phosphorylation, the release of heat, and a rise in metabolic rate [49]. MH presents with hyperthermia, tachycardia, hypercarbia, increased oxygen consumption, and muscle rigidity following the administration of a volatile anesthetic or depolarizing muscle relaxants. In the ED, MH is most likely to present following an intubation using succinylcholine and MH should be a diagnostic consideration in a patients with acute decompensation following intubation. MH is treated with intravenous dantrolene loaded at a dose of 2.5 mg/kg followed by boluses of 1 mg/kg until symptoms resolution [48]. Aggressive cardiopulmonary support, maintenance of normothermia and euvolemia, and treatment of electrolyte derangements is likewise important.

#### **3.4 Salicylate toxicity**

Aspirin ingestion is the most common cause of salicylate toxicity, but other common sources include Oil of Wintergreen, some wart removers, and keratolytics [50]. Salicylate toxicity is an important sepsis mimic, as patients with salicylate toxicity will have tachycardia, tachypnea, elevated temperature, and lactic acidosis. These symptoms occur secondary to salicylate interference with aerobic metabolism [50]. The classically described triad of salicylate toxicity is hyperpnea, tinnitus, and gastrointestinal irritation [51]. Gastrointestinal symptoms vary and can include abdominal pain, nausea, vomiting, and diarrhea. Tinnitus associated with salicylate toxicity may be described as hearing loss rather than "ringing in the ears" by patients and may be a difficult symptom to elicit if the patient is altered or obtunded [51]. Laboratory testing in salicylate toxicity will show a classic "triple acid-base disorder." This includes a respiratory alkalosis from hyperventilation, a compensatory non-gap metabolic acidosis, and an anion-gap metabolic acidosis from secondary to lactic acid accumulation [51]. Management is through systemic alkalinization with sodium bicarbonate [52].

#### **3.5 Anticholinergic toxicity**

Anticholinergic substances are ubiquitous in both pharmaceutical compounds and nature. Commonly encountered causes of anticholinergic toxicity include ingestion of antihistamine medications, tricyclic antidepressants, jimson weed, and tainted recreational drugs. Anticholinergic toxicity can easily be mistake for sepsis,

**27**

*Evaluation and Treatment of Elevated Temperature in the Emergency Department*

anticholinergic toxicity under the consultation of a toxicologist [54].

metic toxicity and withdrawal from antisympathetic agents [55].

spectrum empiric antibiotics should be administered.

**3.7 Thyroid storm**

**3.8 Heat stroke**

as these patients present with high temperature, delirium, and tachycardia [53]. A distinguishing feature of anticholinergic toxicity is the presence of anhidrotic hyperthermia, in contrast to septic patients who are febrile and diaphoretic [53]. This is a result of anticholinergic blockade of sweat glands, preventing homeostatic hydrosis in response to elevated core temperature [53, 54]. Other clinical findings in anticholinergic toxicity include dry mucus membranes, dilated, non-reactive pupils and urinary retention [53]. The management of anticholinergic toxicity is primarily supportive. Benzodiazepines should be used for agitation or seizures [54]. Physostigmine, an anticholinesterase inhibitor, can be used as an antidote for

**3.6 Sympathomimetic toxicity or withdrawal from sympathetic antagonists**

Overstimulation of the sympathetic nervous system can occur through direct agonism of the sympathetic receptors or withdrawal from substances that act as sympathetic antagonists [55]. Common sympathomimetic compounds encountered in the ED include cocaine, phencyclidine, and amphetamines. Withdrawal from alcohol or benzodiazepines can also result in sympathetic overstimulation [56]. Symptoms of sympathomimetic toxicity hyperthermia, tachycardia delirium, and reactive mydriasis [55]. Hyperthermia in sympathetic overstimulation results from direct agonism of alpha receptors as well as heat released by associated psychomotor agitation [55]. Benzodiazepines are mainstay of management of both sympathomi-

Thyroid storm is the most severe manifestation of thyrotoxicosis and can be caused by overdose of therapeutic thyroid hormone or may present in patients with underlying thyrotoxicosis, seemingly unprovoked or may be precipitated by trauma, infection, childbirth, or other acute events [57]. Symptoms of thyroid storm include delirium, hyperthermia, diarrhea, and tachydysrhythmias, which can be severe enough to cause cardiovascular collapse and hemodynamic compromise [57, 58]. Liver failure may also occur [57]. The diagnostic laboratory abnormality in thyroid storm a severely low or undetectable thyroid stimulating hormone (TSH). Physical examination findings concerning for thyroid storm are those classically seen in hyperthyroidism and include ophthalmopathy, lid lag, thyromegaly, hand tremor, and global hyperreflexia [57, 58]. ED management of includes immediate treatment with a beta blocker, a thionamide, and glucocorticoids [59]. An iodine preparation should be given an hour after the administration of the thionamide, to prevent the iodine being used as substrate for the synthesis of more thyroid hormone [59]. If an infection is suspected as the cause of thyroid storm, broad-

Heat stroke is condition of elevated core body temperature with associated central nervous system dysfunction, commonly encephalopathy [60]. Heat stroke can be broadly divided into non-exertional and exertional. Non-exertional heat stroke classically affects older individuals with comorbidities that result in impaired thermoregulation, prevent access to adequate hydration, or inhibit removal from a hot environment [60]. In contrast, exertional heat stroke is more likely to occur in young, healthy individuals in the setting of exertion that overwhelms homeostatic thermoregulatory mechanisms. Heat stroke is a clinical diagnosis of exclusion made

*DOI: http://dx.doi.org/10.5772/intechopen.94899*

*Evaluation and Treatment of Elevated Temperature in the Emergency Department DOI: http://dx.doi.org/10.5772/intechopen.94899*

as these patients present with high temperature, delirium, and tachycardia [53]. A distinguishing feature of anticholinergic toxicity is the presence of anhidrotic hyperthermia, in contrast to septic patients who are febrile and diaphoretic [53]. This is a result of anticholinergic blockade of sweat glands, preventing homeostatic hydrosis in response to elevated core temperature [53, 54]. Other clinical findings in anticholinergic toxicity include dry mucus membranes, dilated, non-reactive pupils and urinary retention [53]. The management of anticholinergic toxicity is primarily supportive. Benzodiazepines should be used for agitation or seizures [54]. Physostigmine, an anticholinesterase inhibitor, can be used as an antidote for anticholinergic toxicity under the consultation of a toxicologist [54].

#### **3.6 Sympathomimetic toxicity or withdrawal from sympathetic antagonists**

Overstimulation of the sympathetic nervous system can occur through direct agonism of the sympathetic receptors or withdrawal from substances that act as sympathetic antagonists [55]. Common sympathomimetic compounds encountered in the ED include cocaine, phencyclidine, and amphetamines. Withdrawal from alcohol or benzodiazepines can also result in sympathetic overstimulation [56]. Symptoms of sympathomimetic toxicity hyperthermia, tachycardia delirium, and reactive mydriasis [55]. Hyperthermia in sympathetic overstimulation results from direct agonism of alpha receptors as well as heat released by associated psychomotor agitation [55]. Benzodiazepines are mainstay of management of both sympathomimetic toxicity and withdrawal from antisympathetic agents [55].

### **3.7 Thyroid storm**

*Trauma and Emergency Surgery - The Role of Damage Control Surgery*

one of the symptom complexes outlined below (**Table 4**).

Hypertonia, temperature > 38°C AND ocular OR inducible clonus

**3.3 Malignant hyperthermia (MH)**

*Hunter criteria for serotonin syndrome [47].*

Inducible clonus AND agitation OR diaphoresis Ocular clonus AND agitation OR diaphoresis

Spontaneous clonus

**Table 4.**

Tremor AND hyperreflexia

**3.4 Salicylate toxicity**

alkalinization with sodium bicarbonate [52].

**3.5 Anticholinergic toxicity**

Suspect serotonin syndrome if the patient has taken a serotonergic agent and has

MH is a genetic disorder which results in a hypermetabolic response to volatile anesthetics and depolarizing muscle relaxants [48]. This pathologic response to these medications results from caused the release of excessive calcium from the sarcoplasmic reticulum, which leads to uncoupling of oxidative phosphorylation, the release of heat, and a rise in metabolic rate [49]. MH presents with hyperthermia, tachycardia, hypercarbia, increased oxygen consumption, and muscle rigidity following the administration of a volatile anesthetic or depolarizing muscle relaxants. In the ED, MH is most likely to present following an intubation using succinylcholine and MH should be a diagnostic consideration in a patients with acute decompensation following intubation. MH is treated with intravenous dantrolene loaded at a dose of 2.5 mg/kg followed by boluses of 1 mg/kg until symptoms resolution [48]. Aggressive cardiopulmonary support, maintenance of normothermia and euvolemia, and treatment of electrolyte derangements is likewise important.

Aspirin ingestion is the most common cause of salicylate toxicity, but other common sources include Oil of Wintergreen, some wart removers, and keratolytics [50]. Salicylate toxicity is an important sepsis mimic, as patients with salicylate toxicity will have tachycardia, tachypnea, elevated temperature, and lactic acidosis. These symptoms occur secondary to salicylate interference with aerobic metabolism [50]. The classically described triad of salicylate toxicity is hyperpnea, tinnitus, and gastrointestinal irritation [51]. Gastrointestinal symptoms vary and can include abdominal pain, nausea, vomiting, and diarrhea. Tinnitus associated with salicylate toxicity may be described as hearing loss rather than "ringing in the ears" by patients and may be a difficult symptom to elicit if the patient is altered or obtunded [51]. Laboratory testing in salicylate toxicity will show a classic "triple acid-base disorder." This includes a respiratory alkalosis from hyperventilation, a compensatory non-gap metabolic acidosis, and an anion-gap metabolic acidosis from secondary to lactic acid accumulation [51]. Management is through systemic

Anticholinergic substances are ubiquitous in both pharmaceutical compounds and nature. Commonly encountered causes of anticholinergic toxicity include ingestion of antihistamine medications, tricyclic antidepressants, jimson weed, and tainted recreational drugs. Anticholinergic toxicity can easily be mistake for sepsis,

**26**

Thyroid storm is the most severe manifestation of thyrotoxicosis and can be caused by overdose of therapeutic thyroid hormone or may present in patients with underlying thyrotoxicosis, seemingly unprovoked or may be precipitated by trauma, infection, childbirth, or other acute events [57]. Symptoms of thyroid storm include delirium, hyperthermia, diarrhea, and tachydysrhythmias, which can be severe enough to cause cardiovascular collapse and hemodynamic compromise [57, 58]. Liver failure may also occur [57]. The diagnostic laboratory abnormality in thyroid storm a severely low or undetectable thyroid stimulating hormone (TSH). Physical examination findings concerning for thyroid storm are those classically seen in hyperthyroidism and include ophthalmopathy, lid lag, thyromegaly, hand tremor, and global hyperreflexia [57, 58]. ED management of includes immediate treatment with a beta blocker, a thionamide, and glucocorticoids [59]. An iodine preparation should be given an hour after the administration of the thionamide, to prevent the iodine being used as substrate for the synthesis of more thyroid hormone [59]. If an infection is suspected as the cause of thyroid storm, broadspectrum empiric antibiotics should be administered.

#### **3.8 Heat stroke**

Heat stroke is condition of elevated core body temperature with associated central nervous system dysfunction, commonly encephalopathy [60]. Heat stroke can be broadly divided into non-exertional and exertional. Non-exertional heat stroke classically affects older individuals with comorbidities that result in impaired thermoregulation, prevent access to adequate hydration, or inhibit removal from a hot environment [60]. In contrast, exertional heat stroke is more likely to occur in young, healthy individuals in the setting of exertion that overwhelms homeostatic thermoregulatory mechanisms. Heat stroke is a clinical diagnosis of exclusion made

based on elevated body temperature (generally >40°C), central nervous system dysfunction (classically encephalopathy), and a history of exposure to severe environmental heat or excessive exertion [60]. Evaporative and convective cooling are the treatments of choice and should be initiated as soon as the diagnosis is made to improve morbidity and mortality [61, 62]. Common cooling methods used in the ED include ice water immersion, cooled fluid lavage, and evaporative cooling [61, 62]. In cases of refractory hyperthermia, dantrolene can be used as salvage therapy but its efficacy in this clinical context is uncertain [63, 64].
