Extreme Hyperpyrexia Research Articles

Unraveling quad fever: Severe hyperthermia after traumatic cervical spinal cord injury

PurposeThere are many infectious and inflammatory causes for elevated core-body temperatures, though they rarely pass 40 ℃ (104 ℉). The term “quad fever” is used for extreme hyperpyrexia in the setting of acute cervical spinal cord injuries (SCIs). The traditional methods of treating hyperpyrexia are often ineffective and reported morbidity and mortality rates approach 100%. This study aims to identify the incidence of elevated temperatures in SCIs at our institution and assess the effectiveness of using a non-invasive dry water temperature management system as a treatment modality with mortality. MethodsA retrospective analysis of acute SCI patients requiring surgical intensive care unit admission who experienced fevers ≥ 40 ℃ (104 ℉) were compared to patients with maximum temperatures < 40 ℃. Patients ≥18 years old who sustained an acute traumatic SCI were included in this study. Patients who expired in the emergency department; had a SCI without radiologic abnormality; had neuropraxia; were admitted to any location other than the surgical intensive care unit; or had positive blood cultures were excluded. SAS 9.4 was used to conduct statistical analysis. ResultsOver the 9-year study period, 35 patients were admitted to the surgical intensive care unit with a verified SCI. Seven patients experienced maximum temperatures of ≥ 40 ℃. Six of those patients were treated with the dry water temperature management system with an overall mortality of 57.1% in this subgroup. The mortality rate for the 28 patients who experienced a maximum temperature of ≤ 40 ℃ was 21.4% (p = 0.16). ConclusionThe diagnosis of quad fever should be considered in patients with cervical SCI in the presence of hyperthermia. In this study, there was no significant difference in mortality between quad fever patients treated with a dry water temperature management system versus SCI patients without quad fever. The early use of a dry water temperature management system appears to decrease the mortality rate of quad fever.

Sindrom diskinezija-hiperpireksija – novo hitno stanje kod Parkinsonove bolesti: prikaz slučaja

Aim: Dyskinesia-hyperpyrexia syndrome is a rare case of medical emergency in Parkinson's disease caused by excessive dopaminergic stimulation. It is characterized with severe continuous dyskinesias associated with rhabdomyolysis, hyperthermia, and subsequent alteration of the mental state. The aim of this paper is to present a clinical case of a patient suffering from Parkinson's disease presenting with dyskinesia and hyperpyrexia. Case report: We present a case of a fifty-five-year-old patient who presented with fifteen-day high body temperature and worsening of dyskinesia. The patient, in spite of a detailed clinical examination and laboratory examination, was unidentified as such. In the further course of the treatment, the condition of the patient deteriorated in the sense of extreme hyperpyrexia with the development of respiratory insufficiency and circulatory instability. After four weeks of treatment in the Intensive Care Unit, a patient with severe autonomic dysfunction, passed away. Conclusion: This case points out the importance of early recognition of dyskinesia and hyperpyrexia as an emergency in Parkinson's disease with the aim of early medical support and the prevention of life-threatening consequences.

Extreme Hyperpyrexia of Uncertain Origin

BackgroundThe definition of hyperpyrexia is currently limited to temperatures reaching 106.7°F. A wide range of etiologies have been identified in the literature for an insidious onset of hyperpryexia, however a rapid ascent higher than temperatures of 106.7°F has never been reported nor evaluated. We present the case of a young paraplegic who developed an extreme hyperpyrexia, which to our knowledge is the highest occurring temperature reported in contemporary medical literature. He had a number of medical conditions, none of which are known to produce fever. Why Should an Emergency Physician Be Aware of This?Fever, although a common presentation in the ER in the presence of various symptoms and comorbidities can obscure the diagnosis and lead to unwarranted evaluations. As such this patients case identifies a diagnosis of a fatal ascension of fever.

Dextromethorphan-monoamine oxidase inhibitor interaction in rabbits.

Abstract Severe toxic reactions may occur clinically when imipramine, pethidine or dextromethorphan is administered to a patient being treated with a monoamine oxidase inhibitor (MAOI). Previous reports indicate that imipramine or pethidine produces symptoms characterized by motor restlessness, tremor, extreme hyperpyrexia and death when administered to phenelzine-pretreated rabbits. The present study shows that dextromethorphan (5 mg kg−1) produces identical symptoms in rabbits pretreated with phenelzine sulphate (30 mg kg−1) or nialamide HCl (50 mg kg−1) 42 and 18 h before temperature recording. The dextromethorphan-MAOI interaction appears to be due to a 5-hydroxytryptamine potentiation. In the unanaesthetized cat nictitating membrane preparation, dextromethorphan (5 mg kg−1) markedly enhanced the response of noradrenaline and 5-HT but antagonized the effects of tyramine. This suggests that dextromethorphan blocks the uptake of these amines in the adrenergic nerve endings.

The treatment and management of neuroleptic malignant syndrome

Gratz, Silvia S., Douglas F. Levinson and George M. Simpson. The Treatment and Management of Neuroleptic Malignant Syndrome. Prog. Neuro. Psychopharmacol. & Biol. Psychiat. 1992, 16(4):425–443. 1. 1. The neuroleptic malignant syndrome was initially described as a disorder specifically related to neuroleptic usage with frequent fatal outcome. The observations of variant or mild cases of this syndrome as well as case reports on neuroleptlc-malignant-like syndromes in the absence of neuroloptics raises the issue of the usefulness of this terminology and highlights the potential for inappropriate management of this “malignant” syndrome. It has been suggested that hypothalamic thermoregulatory responses may involve an interplay among noradrenergic, cholinergic and serotonergic pathways. Out treatment strategy is based on the pharmacology of neuroleptics and empirical data, verified in our own clinical practice and considers that it is often difficult to determine whether certain physiologic states are a consequence to or specific triggering factors. 2. 2. If a patient's temperature is less than 101, we emphasize vigorous treatment with anticholinergic agents, while simultaneously assessing the psychiatric need for neuroleptics versus medical risks. Given that the severe rigidity of NMS represents severe extrapyramidal effects of dopamine blockade, there is no reason to withhold anticholinergics in the absence of higher temperatures. Neuroleptics can be stopped at the discretion of the clinician even during circumstances when there is fever below 101. 3. 3. In cases of severe EPS with fever greater than or equal to 101, we recommend stopping neuroleptlcs, treating with anticholinergics and starting with dopamine agonists. In the event of a poor response to dopamine agonists, a brief trial of dantrolene and/or benzodiazepines is recommended. Dantrolene should not be introduced for prolonged periods, since abnormal liver function studies have been observed in approximately 1.8% of patients. 4. 4. In cases of extreme hyperpyrexia (fever greater than 103), clinicians should consider transfer to an ICU or another medical support. Extreme temperatures have been associated with potentially irreversible cerebellar or other brain damage, if not aggressively treated. If neuroleptlcs are later indicated, a 2 week interval after resolution of symptoms should be maintained before reinstituting neuroleptics. 5. 5. In patients with severe EPS without fever, we emphasize aggressive use of anticholinergic therapy, while simultaneously considering the psychiatric need for neuroleptics versus medical risks. In an cases where a patient's swallowing, respirations or physical mobility is severely compromised, we suggest stopping neuroleptlcs. Anticholinergic agents should be continued for 7 days after neuroleptics are stopped. If anticholinergic agents are unsuccessful after 2–3 dosages, dopamine agonlsts may be added, while simultaneously monitoring vital signs. It should be emphasized that severe EPS sometimes takes days to improve even after neuroleptic cessation and the addition of anticholinergics. 6. 6. If EPSs are intense or of long enough duration and, particularly, in the presence of akathisia and agitation, then a combination of excess heat production and interference with the hypothalamic temperature control mechanisms can produce a syndrome of NMS. If EPSs are avoided, neuroleptlcs are used in low dosages and benzodiazepines are used concomitantly for agitation, then we should see very little of NMS.

Management of Otolaryngic Patients Susceptible to Malignant Hyperthermia Without Dantrolene

Malignant hyperthermia (MH) is an adverse reaction most frequently associated with the administration of halogenated inhalational anesthetic agents and the depolarizing muscle relaxant succinylcholine. Characteristic findings are a hypermetabolic state accompanied by extreme hyperpyrexia, acidosis, rhabdomyolysis, and generalized muscle rigidity, often involving the masseter muscles. Dantrolene sodium, which was approved in 1979 by the FDA for use in the prevention of MH in high-risk patients, has neurologic and gastrointestinal side effects. At the Children's National Medical Center (CNMC), 24 children identified as being at risk for the development of a MH reaction were anesthetized for otolaryngic procedures by using "non-triggering" anesthetics and without use of dantrolene sodium. These patients represent 56% of all patients at risk for MH or masseter muscle rigidity (MMR) reactions during an 8-year period at the CNMC. There were no complications. Concomitant muscle biopsies were performed, and caffeine/halothane contracture studies were completed in 18 of these patients, demonstrating 11 susceptible or equivocal responses. The data suggest that children undergoing common otolaryngic procedures who are at risk for development of MH may be safely anesthetized without the use of prophylactic dantrolene sodium.

Extreme hyperpyrexia in childhood: Presentation similar to hemorrhagic shock and encephalopathy : Caspe WB, Nucci AT, Sangho C. Clin Pediatr. 1989;28:76–80

Extreme hyperpyrexia in childhood: Presentation similar to hemorrhagic shock and encephalopathy : Caspe WB, Nucci AT, Sangho C. Clin Pediatr. 1989;28:76–80

Ethoheptazine-monoamine oxidase inhibitor interaction in rabbits.

Previous reports indicate that meperidine but not morphine produces a marked hyperpyrexia and death in monoamine oxidase inhibitor (MAOI) pretreated rabbits. Since this interaction may be predictive of a serious clinical drug–drug interaction, several other narcotic or structurally related agents were similarly tested in this study. Ethoheptazine citrate (10 mg/kg i.v.), whose chemical structure closely resembles that of meperidine, was found to produce extreme hyperpyrexia and death in rabbits pretreated with an MAOI, phenelzine sulfate (30 mg/kg i.p.), 42 and 18 h prior to temperature recording. This interaction appears to be due to an exaggerated 5-hydroxytryptamine effect. Of the other drugs tested, methadone was found to be inconsistent in its actions whereas anileridine alphaprodine, piminodine, dextropropoxyphene, levorphanol, levallorphan, codeine, and nalorphine were shown to be inactive.

Hypothermia in the Treatment of Acute Pancreatitis

A hypothermic unit was used to reduce and control extreme hyperpyrexia in two patients with acute pancreatitis. Both survived. Recent experiences by others using hypothermia in the treatment of experimental pancreatitis give us a rational explanation for the good response in both patients. The encouraging results obtained with a hypothermic unit as a basic therapeutic modality in severe cases of pancreatitis warrant additional clinical trials.

Experiences with postoperative temperatures above 108 °F: Use of hypertonic glucoses

T HE occurrence of exceptionaIIy high temperature in the surgica1 patient is of sufficient frequency to warrant a review of our own reactions to the probIem and its management. In such instances death ensues mainIy as a direct resuIt of fever and not the underIying pathoIogic condition. That patients can survive temperatures over 108’F. with fuII recovery has been shown repeatedIy.1-5 Experimenta1 work shows that Iiving tissue does not become irreversibIy damaged until the temperature reaches I I$‘F.~ It is the purpose of this paper to point out that if we can tide these patients over the temperature crisis, they wiI1 have more time to combat their diseases and a certain number wouId survive who wiI1 otherwise be Iost. A review of the physioIogic changes and a IogicaI pIan of treatment is therefore presented. The genera1 picture in extreme hyperpyrexia is one of marked metaboIic aIteration. The basa1 metaboIic rate is often +so to + 75 in severe cases. Such a sudden increase in metaboIism puts a severe strain on the resources of the body which, as we shaI1 see, are aIready overtaxed.7-g Thus oxygen is in great demand but is suppIied with diffIcuIty, for it has been shown that the oxygen tension of arteria1 bIood is materiaIIy reduced in cases of high fever.10a11 The puIse rate is increased from five to ten beats per minute for each degree rise in temperature (Fahrenheit). Later it becomes so rapid that insufflcient cardiac output occurs. The bIood pressure first rises and Iater faIIs to shock IeveIs, indicating inabiIity to cope with the situation. The blood voIume is progressively diminished due to Ioss of water by the skin and Iungs, and Iater by the advent of shock.12-14 The bIood becomes concentrated. When tissue fluid loss into the bIoodstream exceeds 5 cc. per kg. per hour, periphera1 coIlapse ensues. Progressive dehydration together with the high metaboIic rate then increases the body temperature even more, constituting a deadIy cycIe. As fever increases, the ganglion ceIIs of the centra1 nervous system shrink,16 tota chIorides faII,16 the CO2 content of the bIood is Iowered, the Iactic acid content of the bIood is increased by 30 to 78 per cent above normaI,” base is mobiIized from the tissues to the bIood, the bIood sugar rises early then faIIs as supplies become depleted and the non-protein nitrogen rises. The inorganic phosphorus faIIs due to the greatIy increased rate of gIucose utiIization. The earIy rise in blood sugar is dependent upon the Iiver which is so stimuIated in high fever to reIease sugar that it often overshoots its mark. Hypersecretion of insuIin and epinephrine occurs.1s These changes favor glycogenoIysis to meet the demand for fue1, unti1 the Iiver is depIeted of its gIycogen and disaster is at hand. Autopsy at this time reveaIs a marked decrease in Iiver gIycogen. In addition Iiver function becomes deficient as a resuIt of hyperpyrexia per se.1v--22 This is unfortunate inasmuch as the demands made upon the Iiver at this time demand a very efficient response. Thus jaundice, hepatomegaIy and Iiver faiIure have been noted foIIowing therapeutic hyperpyrexia.1g-21 The serum aIbumin and fibrinogen IeveIs faI1, again due to impaired Iiver function. AS a resuIt of insuffIcient avaiIabIe gIucose, proteins and fats are burned with remarkabIe rapidity to suppIy fueI.23-27 Thus incompIete fat combustion occurs and ketonuria is observed. Protein metaboIism is so aItered that more than 25 gm. may be burned per hour. GIucose may thus be considered as a protein and fat sparer. WhiIe these changes are taking pIace, the cardiopuImonary circuit is Iaboring desper-

Extreme Hyperpyrexia with Recovery

Extreme Hyperpyrexia with Recovery

A note on the management of gunshot wounds of the head in civil practice

1. 1. In gunshot wounds of the head the aim is to prevent intracerebral infection and to minimize undesirable post-traumatic sequelae. Debridement and removal of dead brain tissue, foreign particles, shattered pieces of bone and the bullet (if possible) will help toward this end. Shock should always be treated first even if this takes twenty-four to thirty-six hours. 2. 2. The state of consciousness is of prognostic importance. Patients conscious on entrance or soon after represent the most favorable class for recovery, irrespective of extent of apparent trauma. In this group recovery obtained in about 80 per cent. Among those in deep coma death occurred either soon after entrance (rapid collapse) or after the first twelve to fifteen hours from extreme hyperpyrexia and increased intracranial pressure (hyperpyrexic death). 3. 3. In the absence of skull injury, damage to the intracranial contents should not be dismissed as a possibility. An example of subdural hemorrhage with no fracture or perforation of the skull is given.