Pyrexia - PACT - ESICM

More documents

Recommendations

Info

Task 4. Understanding and treating fever Although fever can be regarded as a beneficial component of the host response to invading micro-organisms and tissue injury, deleterious endocrine and metabolic side effects can occur, including increased protein breakdown (catabolism) and cerebral damage. The latter is imminent when temperature exceeds 42 °C for one hour or longer. The effect of raised ambient temperature on the endocrine and metabolic response is displayed in the figure: Fever is normally good for the patient but can be bad Responses of different organs to fever From: Dimopoulos G, Falagas M. Approach to the febrile patient in ICU. Infect Dis Clin North Am 2009;23:471–484 A warm nursing environment (e.g. a fluidised bed at 32 °C) after trauma, burns or surgery, for instance, may attenuate these effects. The diminished gradient between body and ambient temperature decreases heat production, metabolic stress and the catabolic response. See the following reference: Ryan DW, Clague MB. Nitrogen sparing and the catabolic hormones in patients nursed at an elevated ambient temperature following major surgery. Intensive Care Med 1990; 16(5): 287–290. PMID 2212251 A number of exogenous stimuli (e.g. infections, inflammatory or autoimmune diseases, vascular occlusive diseases, drugs) lead to the release of large proteins called ‘endogenous pyrogens’ which bind to specific receptors in the preoptic region of the anterior hypothalamus where a blood-brain barrier acts as a valve permitting the entrance of a limited quantity of these proteins into the brain. Pyrogen access and contact with neurons is achieved with the aid of small neuronal cells with fenestrated capillaries called ‘circumventricular organs’. [40]
Task 4. Understanding and treating fever This results in a direct response of the neurons within the organum vasculosum of the lamina terminalis or of the astrocytes or microglia to circulating cytokines such as interleukin-1 and -6, resulting in arachidonic acid metabolite production (prostaglandin E2 and thromboxane A2) and upregulation of the thermostatic set point. The brain responds by sending signals that activate effector mechanisms (through the spinal/supraspinal motor system or throughout the sympathetic nervous system), which in turn generate heat production (in brown adipose tissue), reduce heat loss and increase core body temperature to match the upregulation of the thermostatic set point (see diagram). The activation of arachidonic acid metabolites acts as a substrate for the cyclooxygenase-2 (COX-2) pathway, which in turn leads to further elevation of prostaglandin levels, a decreased rate of firing of sensitive neurons and an increased heat production. The role of COX-2 is important for the development of fever although its activity is inhibited by selective inhibitors, namely nonsteroidal anti-inflammatory drugs (NSAIDS) and acetaminophen. Thermal imbalance may of course occur in the absence of a reset of the thermostat, when heat loss is less than heat production as, for example, in hyperthyroidism, salicylate and anticholinergic drug overdose, skin disease and heat stroke. Saper CB, Breder CD. The neurologic basis of fever. N Engl J Med 1994; 330(26): 1880–1886. PMID 7832832 Luheshi GN. Cytokines and fever. Mechanisms and sites of action. Ann N Y Acad Sci 1998; 856: 83–89. PMID 9917868 Simmons DL, Wagner D, Westover K. Nonsteroidal anti-inflammatory drugs, acetaminophen, cyclooxygenase 2, and fever. Clin Infect Dis 2000; 31 Suppl 5: S211–218. PMID 11113025 Leon LR. Invited review: Cytokine regulation of fever: studies using gene knockout mice. J Appl Physiol 2002; 92(6): 2648–2655. PMID 12015385 The following figure illustrates the time course of thermostat resetting and the consequences for the time course of body temperature (green line) as a function of heat gain, when the thermostat is set at a higher level (grey line), and of heat [41]
Page 1 and 2: AN ESICM MULTIDISCIPLINARY DISTANCE
Page 3 and 4: LEARNING OBJECTIVES After studying
Page 5 and 6: Introduction INTRODUCTION Thirty pe
Page 7 and 8: Task 1. Assessing and measuring fev
Page 19 and 20: Task 2. Determining the cause of fe
Page 35 and 36: Task 3. Fever in specific categorie
Page 39 and 40: Fever in neurological disease Task
Page 43: Task 4. Understanding and treating
Page 47 and 48: Task 4. Understanding and treating
Page 49 and 50: Task 4. Understanding and treating
Page 51 and 52: Self-assessment EDIC-style Type A 8
Page 53 and 54: Self-assessment Self-assessment ans
Page 55 and 56: Patient Challenges Q. Outline the p
Page 57 and 58: Patient Challenges A cardiogenic ca
Page 59 and 60: Patient Challenges Cooling techniqu
Page 61 and 62: syndrome was clear and antibiotics,
Page 63 and 64: Patient Challenges An 18-year-old m
Page 65: Patient Challenges often a transien

Pyrexia - PACT - ESICM

Create successful ePaper yourself

Delete template?

Save as template?