August 09, 2010

FEVER, HYPERTHERMIA AND HYPOTHERMIA

FEVER

most common complaint; usually self-managed; not always due to infection

a state of elevated core temperature, which is often, but not necessarily, part of the defensive responses of the multicellular organism (host) to the invasion of the live microorganisms or inanimate matter recognized as pathogenic or alien by the host (from the International Union of Physiological Sciences Commission for Thermal Physiology, 2001)

elevation of the body temperature above the normal circadian range in response to a new temperature set point that has been established in the thermoregulatory center located in the hypothalamus

inc. Hypothalamic set point activation of vasomotor center vasoconstriction (shunting of blood from the periphery to the internal organs) dec heat loss from skin person feels cold shivering or non shivering heat production temp of blood surrounding hypothalamus = new set point continuous febrile state dec. in pyrogen conc. Or antipyretics downward reset of hypothalamic set point

hyperprexia

fever of > 41.5 degrees celcius due to severe infections or CNS hemorrhages normally a normal thermal ceiling of 106 degrees farenheit is observed, this is mediated by neuropeptides (central antipyretics)

FEBRILE RESPONSE

complex physiologic reaction to disease, involving not only cytokine-mediated rise in core temperature but also the generation of acute phase reactants, and the activation of numerous physiologic, endocrinologic and immunologic systems (tachycardia, tachypnea, hypotension, oliguria)

- Physiologic means that aside from a high temperature, you would expect your patients to have competitor response= Heart rate, respiratory rate, basal metabolic rate.

Endocrinologic, catecholamines= heart rate, glucagon

- Immunologic System, blood will respond to febrile reaction and there will be an increase in inflammatory cells(WBC).

The anterior hypothalamus acts as the heat-loss center. The posterior hypothalamus acts as the heat-producing center.

Can be caused by: exogenous pyrogens lipopolysaccharide endotoxin, outside the body endogenous pyrogens induced by exogenous pyrogens interleukin-1, TNF prostaglandin E2 in CNS: raises hypothalamic set point in peripheral tissues: causes myalgia, arthralgia

Fever results when exogenous pyrogens (bacteria, viruses, fungi, other microorganisms, allergens, etc.) or pyrogenic factors (immune complex, lymphokines from sensitized lymphocytes, etc.) encounter circulating monocytes and monocyte-derived tissue macrophages, the major sources of biologically defined endogenous pyrogens. Endogenous pyrogens increase prostaglandin synthesis, which stimulates the thermostat center, thereby elevating the set point. Elevation of the set point steps up the mechanisms of heat production and conservation and inhibits the mechanisms for heat loss. The endogenous pyrogens include interleukin-1 ( and ), inerleukin-2, tumor necrosis factor ( and ) and interferon .

The physiologic response to fever may be adequate or inadequate. In the immunocompetent, other symptoms will be present aside from fever.Error! Objects cannot be created from editing field codes.

HYPERTHERMIA

unchanged setting of the thermoregulatory center in conjunction with an uncontrolled increase in body temperature that exceeds the bodys ability to lose heat

can be rapidly fatal and characteristically does not respond to antipyretics (paracetamol or any relative agents)

does not involve pyrogenic molecules

can develop from 24 hours to 48 hours after the operation(drug fever)

Causes of Hyperthermia syndromes

1. Heat stroke caused by thermoregulatory failure in association with a warm environment can be terminal or can be secondary terminal

Exertional caused by exercise in higher-than-normal heat and/or humidity can also be precipitated by dehydration or OTC antihistamines with anticholinergic side effects

Nonexertional occurs in high heat or humidity in patients taking anticholinergics (including antihistamines); antiparkinsonian drugs; diuretics; phenothiazines

2. Drug-induced caused by drugs such as MAO inhibitors, tricyclic antidepressants, amphetamines, cocaine, phencyclidine, LSD, sallicylates, lithium can increase heart rate, and basal metabolic rate

3. Neuroleptic malignant syndrome caused by neuroleptic agents such as phenothiazines, butyrophenones (haloperidol, bromperidol), fluoxetine, loxapine, tricyclic dipenzodiazepines, metoclopramide, domperidone, thioxetine, molindone consists of lead-pipe muscle rigidity, extrapyramidal side effects, autonomic dysregulation, hyperthermia

4. Malignant hyperthermia systemic response to halothane and other inhalational anesthetics in patients with genetic abnormality (in skeletal muscle sarcoplasmic reticulum) increased intracellular Calcium -> increased muscle rigidity -> increased thrombogenesis also in post-operative patients patients prone to develop CV instability and acidosis

5. Serotonin syndrome caused by selective serotonin reuptake inhibitors, monoamine oxidase inhibitors, tricyclic antidepressants additional symptoms: diarrhea, tremor, myoclonus

6. Endocrinopathy caused by thyrotoxicosis, pheochromocytoma increased basal metabolic rate

7. CNS Damage caused by cerebral hemorrhage, status epilepticus, hypothalamic injury

FEVER VS HYPERTHERMIA

Elevated temperature in hyperthermia is NOT decreased by antipyretics

Diagnosis of hyperthermia is difficult but should be considered Events immediately preceding the elevation of core temperature (eg. Heat exposure or treatment with drugs that interfere with thermoregulation) Physical findings of dry skin, hallucinations, delirium, pupil dilation and muscle rigidity

**Factors affecting Heat production a. Basal metabolism b. Muscular activity (voluntary shivering) c. Thyroxin and epinephrine (stimulating effects on metabolic rate) d. Specific dynamic action of food e. Chemical reaction

**Factors affecting Heat conservation a. Vasoconstriction b. Insulation of heat by means of thick clothing

**Factors affecting Heat lossa. Vasodilation (radiation, conduction, convection) b. Evaporation (sweat, insensible water loss) c. Urine and feces

CLINICAL THERMOMETRY

factors that may influence hemostatic measurement:1. Observer variability

2. Anatomic variability:

Oral / tympanic membrane > rectal > axillary

3. Physiologic variability: mean oral temp for healthy people aged 18-40 y/o = 36.8 +/- 0.4 C lowest at 6am = 37.2 C highest at 4-6pm = 37.7 C

*Fever an am temp of >37.2 C or a pm temp of 37.7 C

Types of thermometer oral has a longer probe than rectal gives the most reliable reading placed under the tongue axillary same as oral rectal has a more blunt end tympanic membrane digital- always consider: power source affects the reading calibration must be properly adjusted

EVALUATION OF PATIENTS WITH FEVER

1. status of patient check responsiveness and coherence if not coherent: severe infection check vital signs (BP, HR, RR, temp) ask when the last urination was. monitor urine output. check other signs that would suggest an infection. headache: CNS infection cough (productive) then fever: bacterial pneumonia fever then cough: viral flu dry cough: influenza rashes: dengue

2. requirement for isolation procedures in viral infections

3. requirement for immediate antimicrobial therapy not necessary in viral infections different approach in the immunosuppressed

CLINICAL APPROACH TO THE PATIENT WITH FEVER

Diagnostic Approach

History

1. fever characteristicsa. onset abrupt gradualb. pattern intermittent with normalization and recovery to baseline remittent doesnt go back to baseline even with intake of paracetamoleg, Salmonella, typhoid, bacterial infections continuous or sustained eg, severe infection, CNS, viral relapsing longer periods of afebrile stateeg, vivax, malaria septic or hectic erratic, more exaggerated; can go down to normal with intake of paracetamol

2. chronology of symptoms If fever comes first before dry cough along with muscle pain, and joint pains, there is viral flu If non productive cough occurred first then after 2 days becomes productive with chest pain then it is a bacterial infection like pneumonia

3. antecedent events and precipitating factors underlying medical illness (eg. valvular heat disease, COPD, diabetes) surgical and dental procedures previous or recent hospitalizations prescription drugs, supplements, herbs taken without physicians supervision factors affecting immunologic status (eg, cancer) travel and residential history include locations during military service; travel to Palawan: consider malaria occupational history exposure to animals; toxic fumes; potential sinfectious agents; possible antigens; febrile or infected individuals in the home, workplace, school immunizations flu shot: llocal soreness at injection site + low-grade fever STD exposure family history and ethnicity unusual hobbies dietary proclivities household pets sexual orientation and practices include precautions taken/not taken use of tobacco, marijuana, IV drugs, alcohol drug allergies and hypersensitivities season of the year

Physical Examination

general appearance vital signs signs of toxicity focus of infection skin lesions presence and location of adenopathy presence and morphology of genital, mucosal, or conjunctival lesions detection of hepatosplenomegaly (malaria) presence of arthritis signs of nuchal rigidity, meningismus or neurologic dysfunction rectal exam imperative penis, prostate, scrotum, testes for males pelvic exam part of complete PE of females

Laboratory Tests

1. Tempo and complexicity of work-up depend on: diagnostic considerations pace of illness immune status2. clinical pathology CBC blood smears routine analysis of important body fluids (sputum evaluation, CSF exam) histopathological studies urinalysis joint fluid exam stool exam bone marrow biopsy3. chemistry electrolyte, glucose, BUN, creatinine4. radiology chest x-ray ultrasound CT scan5. microbiological studies most important smears and cultures (throat, urethra, anus, cervix, vagina)

Therapeutic Management- antibiotic therapy when needed- use of antipyretics

1. Fever oral aspirin, acetaminophen (preferred) , NSAIDs glucocorticoids

2. Hyperthermia physical cooling with the use of sponging, cooling blankets, fans, ice baths administration of IV fluids etc gastric or peritoneal lavage w/ iced saline for malignant cases: dantrolene, procainamide, bromocriptine, levodopa, amantidine, nifedipine for muscle paralysis: curare and pancuronium

HYPOTHERMIA

Unintentional drop in the bodys core temperature below 35C (95F) Primary result of the direct exposure of a previously healthy individual to the cold Secondary complication of a serious disorder

RISK FACTORS

A. Age extremes Elderly and neonates are vulnerable to hypothermia1. Elderly diminished thermal perception more susceptible to immobility, malnutrition & systemic illnesses that interfere with heat generation or conservation2. Neonates high rates of heat loss due to their increased surface-to-mass ratio lack of effective shivering & adaptive behavioral responses

B. Environmental exposure Occupational Sports related Inadequate clothing Immersion

C. Drugs and intoxication1. Ethanolcauses vasodilation, which increases heat loss, reduces thermogenesis & gluconeogenesis and may impair judgement or lead to obtundation2. Phenothiazines, barbiturates, benzodiazepines, cyclic antidepressants Reduce centrally mediated vasoconstriction3. Anesthetics Can block shivering responses4. Neuromuscular blockers

D. Endocrine related1. Hypothyroidism particularly when extreme (myxedema coma) reduces metabolic rate & impairs thermogenesis and behavioral responses2. Adrenal insufficiency & hypopituitarism Increase susceptibility to hypothermia3. Hypoglycemia Most commonly caused by insulin or other hypoglycemics Result of neuroglycopenic effects on hypothalamic function4. Uremia, diabetic ketoacidosis & lactic acidosis Can lead to altered hypothalamic regulation

E. Neurologic-related1. Trauma, cerebrovascular accident (ex. Stroke), subarachnoid hemorrhage or hypothalamic lesions increases susceptibility to hypothermia2. Agenesis of corpus callosum, Shapiro syndrome cause of episodic hypothermia characterized by profuse perspiration followed by rapid fall in temperature3. Acute spinal cord injury disrupts autonomic pathways that lead to shivering prevents cold-induced reflex vasoconstrictive responses4. Parkinsons disease

F. Multisystem1. Malnutrition, Trauma2. Sepsis3. Shock4. Hepatic or renal failure Decreased glycogen stores & gluconeogenesis Diminished shivering responses5. Acute myocardial infarction low cardiac output

G. Burns, psoriasis, erythrodermas, & exfoliative dermatologic disorders increased peripheral blood flow excessive heat lossH. Immobility or debilitation

THERMOREGULATION

Preoptic anterior hypothalamus handles thermoregulation

ANS immediate defensea. release of NEb. increased muscle tonec. shivering leading to thermogenesisd. increased basal metabolic ratee. peripheral vasoconstriction

Endocrine system delayed control

CLINICAL APPROACH

A. History1. Exposures2. Underlying diseases/problems3. Other associated symptoms

B. Physical Exam patients may be confused or combative maladaptive behavior

C. Diagnosis Measure the core temperature at 2 sites rectal probe & esophageal probe Sole determination by infrared tympanic thermography not reliable

D. Stabilization process1. Cardiac monitoring along with attempts to limit further heat loss2. If patient is in ventricular fibrillation 1 sequence of 3 fibrillation attempts (2j/kg)3. Supplemental oxygenation leftward shift of oxyHb dissociation curve4. Pulse oxymetry unreliable in patients with vasoconstriction5. Endotracheal intubation if protective airway reflexes are absent6. Prevention of ventricular arrythmias by adequate preoxygenation7. Gastric tube insertion prevents dilatation secondary to decreased bowel motility8. Foley catheter insertion9. Rehydration10. Maintenance of acid-base and electrolyte balance

REWARMING STRATEGIES

A. Passive For acute, mild hypothermia involves covering and insulating the patient in a warm environment usually 0.5 2.0C per hour

B. Active for moderate (28-32C) necessary under the following conditions: cardiovascular instability, age extremes, CNS dysfunction, endocrine insufficiency, or any suspicion of secondary hypothermia

1. External Best accomplished with forced-air heating blankets Prevent use of electric blankets Radiant heat sources / hot packs2. Core Airway rewarming with heated humidified oxygen (40C - 45C) via mask or endotracheal tube

C. Intensive For intense (