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Central Fever: a Challenging Clinical Entity in Neurocritical Care

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Central Fever: a Challenging Clinical Entity in Neurocritical Care eISSN 2508-1349 J Neurocrit Care 2020;13(1):19-31 https://doi.org/10.18700/jnc.190090 Central fever: a challenging clinical entity in neurocritical care Review Article Keshav Goyal, MD, DM1; Neha Garg, MD2; Parmod Bithal, MD3 Received: July 18, 2019 1Department of Neuroanaesthesiology and Critical Care, Neurosciences Centre, All India Institute Revised: December 12, 2019 of Medical Sciences, New Delhi, India Accepted: December 13, 2019 2Institute of Liver and Biliary Science, Delhi, India 3Department of Anesthesiology, King Fahd Medical City, Riyadh, Saudi Arabia Corresponding Author: Keshav Goyal, MD, DM Department of Neuroanaesthesiology and Critical Care, Neurosciences Centre, All India Institute of Medical Sciences, 710, New Delhi 110029, India Tel: +91-11-26588700-4111 E-mail: [email protected] Fever is probably the most frequent symptom observed in neurointensive care by healthcare providers. It is seen in almost 70% of neurocritically ill patients. Fever of central origin was first described in the journal Brain by Erickson in 1939. A significant number of patients develop this fever due to a noninfectious cause, but are often treated as having an infectious fever. Unjustified use of antibi- otics adds to the increased cost of treatment and the emergence of resistant strains, contributing to additional morbidity. Since fever has a detrimental impact on the recovery of the acutely injured brain and contributes to an increased stay in the neurointensive care unit (NICU), timely and accurate diagnosis of the cause of fever in the NICU is imperative. Here, we try to understand the underlying mechanism, risk factors, clinical characteristics, diagnosis and management options of the central fever. We also make an attempt to differentiate two noninfectious causes of fever in the NICU: paroxysmal sympathetic hyperactivity and central fever. Keywords: Humans; Fever; Brain; Intensive care units; Ant-bacterial agents INTRODUCTION ten treated as infectious fever. Unjustified use of antibiotics adds to the increased cost of treatment and the emergence of resistant Fever is probably the most frequent symptom observed in the strains, contributing to additional morbidity. Since fever has a neurointensive care unit (NICU) by healthcare providers. An detrimental impact on the recovery of the acutely injured brain oral temperature greater than 37.5℃ is considered a fever [1,2]. [12-15] and contributes to an increase in length of stay in NICU Hyperpyrexia is usually a diagnosis of exclusion, with tempera- [8]; timely and accurate diagnosis of the cause of fever in the tures exceeding 41℃ and nonresponsiveness to antipyretic treat- NICU is imperative. ment [3,4]. Fever is seen in almost 70% of neurocritically ill pa- Here, we try to understand the underlying mechanism, risk fac- tients [5-10]. Fever of central origin was first described by in the tors, clinical characteristics, diagnosis and management options of journal Brain by Erickson [11] in 1939. A significant number of central fever (CF). We also make an attempt to differentiate two these patients have fever from noninfectious causes (47% in Kil- noninfectious causes of fever in NICU, paroxysmal sympathetic patrick et al. [6] and 25% in Commichau et al. [7]), but this is of- hyperactivity and CF. © 2020 The Korean Neurocritical Care Society This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited. www.e-jnc.org 19 Keshav Goyal, et al. • Central fever EPIDEMIOLOGY minalis, or from hormonal changes (progesterone, prostaglandin) modifying the firing rate of temperature-sensitive neurons in the Overall in the intensive care unit (ICU), at least 50% of fever are medial preoptic nucleus [40]. reported to be due to noninfectious causes [16]. The incidence of Posttraumatic hyperthermia, also known as neurogenic fever, is noninfectious fever in the neurology ICU is 23% while in the neu- another common cause of fever. Stimulation studies have suggest- rosurgical ICU it is 47% [6]. Of these, the highest rates of febrile ed that the mechanism involves an imbalance between the hypo- episodes occur in patients with subarachnoid hemorrhage (SAH; thalamus and the various temperature regulating centers in the 50% to 65%), followed by traumatic brain injury (TBI; 4% to brainstem and spinal cord [41]. Won and Lin [42], in their study 40%) and intracerebral hemorrhage (ICH; 31%), with no cause conducted on rabbits, found that inhibition of five hydroxytrypt- of fever identified in 28% of patients, suggesting fever of central amine receptors in the anterior hypothalamus increased heat pro- origin [7,10,17,18]. Hyperthermia is a frequent complication of duction and decreased heat loss, leading to hyperthermia. Sug- acute ischemic stroke in 50% of these patients and carries a poor gested mechanisms for this effect include increased metabolic prognosis [19]. rate, increased carbon dioxide production, decreased cerebral blood flow, acidosis, brain edema exacerbation, excitotoxic neu- PATHOPHYSIOLOGY rotransmitter release, and blood-brain barrier breakdown. Dis- ease-specific mechanisms are also described in Table 1. An abnormal rise in temperature may be physiological, environ- mental, or even drug-related, rather than due to infection. The Subarachnoid hemorrhage mechanism of CF in the NICU is not well defined but the litera- SAH may cause impairment of hypothalamic thermoregulation ture suggests some probable mechanisms. Inflammatory markers due to the presence of clots in the suprasellar cistern. It may also causing fever may be triggered by extreme physiologic stress in lead to an intense activation of the sympathetic nervous system, acute neurologic injury [20,21]. Brain injury may also lead to the leading to peripheral vasoconstriction and thus diminishing the disruption of the mesencephalic-diencephalic mechanisms re- heat-dissipating mechanisms [43]. sponsible for the inhibition of thermogenesis [22]. Monocytes and macrophages produce the cytokines interleukin 1 (IL-1), IL- Intracerebral hemorrhage 6, and tumor necrosis factor α (TNF-α), which act on the orga- Intraventricular hemorrhage (IVH) is thought to elevate the tem- num vasculosum of laminae terminalis. This in turn leads to the perature set point in the hypothalamus by direct damage to the release of prostaglandin E2 (PGE2) via activation of the cycloox- thermoregulatory centers in the preoptic region, stimulation of ygenase-2 (COX-2) enzyme. PGE2 acts on the preoptic area of prostaglandin production, or decreased inhibitory feedback from the hypothalamus leading to an increase in the set point of the hy- the lower midbrain which suppresses thermogenesis [39]. pothalamus, thereby increasing the body temperature [23-34]. Systemic pyrogens, such as IL-1, appear to enter the brain at re- Tumors gions where there is an incomplete blood-brain barrier (circum- It is hypothesized that a tumor, or its necrotic products, may lead ventricular organs) and act on the preoptic area of the hypothala- to inflammation of leptomeninges, thus triggering fever [44]. mus to induce fever [24,35-38]. Various neurological events that take place in febrile patients affect this pathway. Direct hemotoxic Traumatic brain injury damage to thermoregulatory centers in the preoptic region, inter- While TBI can affect all seven pituitary hormones [45], growth ference with tonic inhibitory inputs from lower midbrain that or- hormone (GH) deficiency is most frequently reported [46,47]. dinarily suppresses thermogenesis, and stimulation of prostaglan- Patients with GH deficiency have a reduced sweating capacity din production leading to temperature set point elevation, have all which increases the risk of developing hyperthermia [48]. TBI-in- been implicated in the causation of CF [39]. CF is speculated to duced hypothalamic-pituitary damage may be due to direct injury result from damage to the hypothalamus, midbrain, or pons, and to the hypothalamic-pituitary area, a secondary injury from hy- be enhanced by increased sympathetic activity, opening of the poxia, or increased intracranial pressure [49]. CF in patients with ventricles, damage to the frontal lobes, physical distortion, diffuse TBI can also be caused by direct injury to the hypothalamus axonal injury (DAI), or toxic blood metabolites [39]. CF may [15,50]. The development of CF is associated with inflammatory also be due to the selective loss of warm-sensitive neurons, the os- changes within the hypothalamus [51]. motic changes detected by the organum vasculosum laminae ter- 20 https://doi.org/10.18700/jnc.190090 Table 1. Various neurological diseases and their relation with central fever Disease Probable mechanisms Risk factors Effects on outcome TBI 1. GH deficiency 1. Diffuse axonal Injury 1. A negative association between early peak fever greater than 39℃ and hospital mortality 2. Direct injury to the hypothalamic-pituitary 2. Frontal lobe injuries 2. Possibility of antibiotic overuse, with the area or secondary injury from hypoxia or associated risk of the emergence of increased intracranial pressure. resistant microorganisms 3. Young age, low GCS on presentation, 3. Prolonged coma or unawareness, diabetes skull fracture, presence of blood in the insipidus and poor outcomes parenchyma/ventricles, and acute brain injury. 4. Location of the skull fracture
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