Edward Walter

The neurological and cognitive consequences of hyperthermia

An elevated temperature has many aetiologies, both infective and non-infective, and while the fever of sepsis probably confers benefit, there is increasing evidence that the central nervous system is particularly vulnerable to damage from hyperthermia. A single episode of hyperthermia may cause short-term neurological and cognitive dysfunction, which may be prolonged or become permanent. The cerebellum is particularly intolerant to the effects of heat. Hyperthermia in the presence of acute brain injury worsens outcome. The thermotoxicity involved occurs via cellular, local, and systemic mechanisms. This article reviews both the cognitive and neurological consequences and examines the mechanisms of cerebral damage caused by high temperature.

The pathophysiological basis and consequences of fever

There are numerous causes of a raised core temperature. A fever occurring in sepsis may be associated with a survival benefit. However, this is not the case for non-infective triggers. Where heat generation exceeds heat loss and the core temperature rises above that set by the hypothalamus, a combination of cellular, local, organ-specific, and systemic effects occurs and puts the individual at risk of both short-term and long-term dysfunction which, if severe or sustained, may lead to death. This narrative review is part of a series that will outline the pathophysiology of pyrogenic and non-pyrogenic fever, concentrating primarily on the pathophysiology of non-septic causes.

Drug-induced hyperthermia in critical care

Fever is common in critically ill patients and the cause is frequently not infection. Drug fevers occur in the intensive care and there are many pharmacological agents, by a variety of mechanisms, which increase body temperature beyond normal range. This article is a review of the common classes of drugs that can induce hyperthermia, highlighting the deleterious effects of a sustained high temperature and outlining available treatments.

Death from Kratom toxicity and the possible role of intralipid

We present the case of a 26-year-old man who was brought into our emergency department in cardiorespiratory arrest, having taken Kratom 24 h previously. Despite multi-organ support, he deteriorated and died from cardiorespiratory failure and hypoxic brain damage 12 h later. Lipid emulsion was given, with significant temporary improvement in the cardiorespiratory failure. Kratom is derived from Mitragyna speciosa, a tropical deciduous and evergreen tree in the coffee family, and is native to Southeast Asia, and its leaves are used as a legal high in some parts of the world. Here, we review the pharmacochemistry of the drug, and wish to highlight that the effects of Kratom may not be as benign as are commonly reported, and the possible role of intralipid in managing the Kratom toxicity in this case.

Management of hyperthermia and hypothermia in sepsis: A recent survey of current practice across UK intensive care units

Sepsis can be associated with either hyperthermia or hypothermia, and various pharmacological and nonpharmacological methods are available in Intensive Care Units (ICUs) tomanage extremes of temperature. Consensus is lacking regarding the optimal target temperatures of patients with sepsis. Observational data from national databases suggest a rise in mortality in patients with temperatures above 40 C and below

Perioperative diagnosis of euglycaemic ketoacidosis

Euglycaemic diabetic ketoacidosis is a term describing features of diabetic ketoacidosis but with normoglycaemia. We present a case of a perioperative diagnosis of euglycaemic ketoacidosis in a patient not known to be diabetic, and the subsequent management of the patient. A 65-year-old lady was scheduled for re-exploration of a giant paraoesophageal hernia, which had been initially repaired over six weeks previously. She developed dysphagia soon after the initial surgery and had low caloric intake. Arterial blood gases performed intraoperatively revealed metabolic acidosis with a normal lactate level. It did not respond to intravenous fluid therapy and sodium bicarbonate. Euglycaemic ketoacidosis was confirmed with raised serum ketone level. Insulin and dextrose infusions were commenced and she was managed in intensive care unit where the metabolic acidosis resolved over a 12-h period.

Management of exertional heat stroke: a practical update for primary care physicians

Exertional heat stroke (EHS) is a risk to athletes, the military, and others undergoing strenuous exertion, especially in temperate climates. It is defined as a core temperature of >40°C with neurological impairment. It is one of the three commonest causes of deaths in athletes, and, untreated, the mortality may be up to 80%. Even when treated, it is associated with significant short- and long-term morbidity. The number of cases of EHS appear to be on the rise; this may be due in part to increasing numbers of athletes participating in endurance events each year. Running USA estimates that 25 000 runners completed a marathon in the US during 1976; by 2016, this had grown to 507 600; similarly, the number of runners completing a half-marathon is estimated to have risen from 303 000 in 1990 to 1 900 000 in 2016.1,2 However, the incidence may also be rising; the US military has reported an eight-fold increase in the rate of hospitalisation from EHS, from 1.8 to 14.5 per 100 000 soldiers, over a 20-year period.3 There are also likely to be a number of runners who do not present to medical services, or in whom the signs are unrecognised. A GP may have contact with athletes in one of three ways: a patient …

The life and work of Harvey Cushing 1869–1939: A pioneer of neurosurgery

Harvey Cushing is well known as being the father of modern neurological surgery and his portrait brands the American Association of Neurological Surgeons. He was the youngest of 10 children and from medical lineage with his father, grandfather and great-grandfather all being general medical practitioners. The details of his life and work are particularly well documented as a result of his obsessive letter writing and record keeping.

The life and work of Rudolf Virchow 1821–1902: “Cell theory, thrombosis and the sausage duel”

After graduating from Friedrich-Wilhelms University in Berlin in 1843, his major work was in pathology, becoming its professor in Pathological Anatomy and Physiology in 1854. He developed an interest in microscopy. His first scientific paper was two years after graduating, on the pathological description of leukaemia, a term he invented. On the back of the recent discovery by Theodor Swann that all animals are composed of cells, he became convinced of their importance, declaring: ‘‘The body is a cell state in which every cell is a citizen. Disease is merely the conflict of the citizens of the state brought about by the action of external forces,’’ and that ‘‘every cell arises from another cell.’’ Virchow was the first to correctly link the origin of cancers from otherwise normal cells, believing that cancer is caused by severe irritation in the tissues (the ‘chronic irritation theory’). Not all of his work was correct, however. He also proposed that cancer spreads around the body by the spread of the irritation in liquid form. And his diagnosis of benign laryngeal ulceration in the German Emperor, Kaiser Friedrich III, prevented the emperor undergoing surgery, who then subsequently died of metastatic laryngeal squamous cell carcinoma. Virchow was accused of malpractice; however, recent reassessment suggests that he was at least partly correct. Virchow was the first to develop a system of autopsy, and an autopsy instrument, for exposing the brain, both still in use today. He was the first to use hair analysis in a criminal investigation, and was the first to describe and name a number of terms, including parenchyma, spina bifida, and vertebral disc rupture, as a result of his work. Virchow’s node, an enlarged left supraclavicular node, is often a sign of gastrointestinal or lung malignancy. Virchow was also wrong in his disbelief of Pasteur’s germ theory of diseases, proposing instead that ‘‘germs seek their natural habitat: diseased tissue, rather than being the cause of diseased tissue.’’ He thought that social factors such as poverty were the major cause of diseases, and that as epidemics were social in origin, the way to combat epidemics was political, not medical. His pathological studies led to further understanding of the mechanism behind venous clot formation, defining his eponymous triad, and the words thrombosis and emboli. He observed: ‘‘The detachment of larger or smaller fragments from the end of the softening thrombus which are carried along by the current of blood and driven into remote vessels. This gives rise to the very frequent process on which I have bestowed the name of Embolia.’’

Manganese toxicity in critical care: Case report, literature review and recommendations for practice

We present the case of a 62-year-old man on the intensive care unit with pancreatitis. Since early in his admission, and for the remainder of his prolonged stay in intensive care, he has received parenteral nutrition for intestinal failure. The whole blood manganese concentration was significantly increased after 2½ months of parenteral nutrition (PN). Three months into his stay, he developed a resting tremor and extra-pyramidal dyskinesia. In the absence of other neurological symptoms, and with no history of essential tremor, Parkinsonism or cerebral signs, hypermanganesaemia was presumed to be the cause. We review manganese metabolism and toxicity in patients who are fed with parenteral nutrition and review the current recommendations and guidelines.