POST OPERATIVE FEVER – SURGEON’S ENVY

Thermoregulation

Balance between heat production and heat loss

Heat production-oxidative process

Catacholamines Thyroxin Increase in substrate load in metabolic

pathway

I/3 of Heat producing activity takes place in muscle mass-increase in muscular activity like exercise or shivering has considerable effect on heat production.

Heat loss

Conduction & Convection

Vasodilatation(transfer of heat from core to surface)

Evaporation – sweating,most important mechanism of heat expenditure

NORMAL BODY TEMP

Normal body temp. 36.2-37.5C(97-99° F) Diurnal variation 0.5 to 1.5 °C (0.9-2.7°F.) Low in morning hours, max in evening Hypothalamus regulates this-input from

temperatura sensitive nerve endings in viscera, skin, temp. sensitive receptors in Ant .Hypothalamus

Temp. regulatory neurons in post hypo alter sweating, by vasoconstriction, vasodilatation and hormonal regulation

Local spinal cord reflexes also regulate vasodilatation, and vasoconstriction.

PATHOGENESIS OF FEVER

FEVER means Heat prod or Decrease heat expenditure Insufficient sweating or by vasoconstriction

Increase Heat production - Elevation of Catecholamines or thyroxin Inappropriate shivering or abnormal muscle

activity.

PYROGENS - A febrile reaction is initiated by pyrogens. May be Exogenous or Endogenous

Classification of Fever

INTERMITTENT (Spiking) Intermittent elevation of temp with regular return to

normal (infection within closed space-abscess)

REMITTENT/FLUCTUATING Continuous type of fever drop in fever without returning to normal-brucellosis, blood stream infections, infected arterial grafts, phlebitis.

UNREMITTING/CONTINUOUSContinuous high fever-CNS injury, pneumonias, typhoidNote: Hydration, Muscle activity, sleep and medication

also alter febrile response.

Altered Febrile Response

AGE; INFANTS HAVE A HIGH TEMP ranging as high as 40.6 OLD AGED Patients - DIMNISHED RESPONSE

MEDICATIONS- NSAID, Steroids-absence of fever

TRAUMA- Fever in trauma is bad sign, trauma to hypothalamus

disturbs thermoregulatory mechanism .

IMMUNOSUPRESSION- Altered production of endogenous leukocyte, pyrogens, lack a febrile response

FEVER IN POST OPERATIVE PATIENT

WIND, WATER, WOUND

FEVER IN POST OPERATIVE PATIENT WIND , WATER, WOUND COMMON CAUSES

ATELACTASIS

VENOUS THROMBOSIS

URINARY TRACT INFECTION

SURGICAL WOUND INFECTION

DAY 1 -2 (24 – 48 HRS.)FIRST DAY FEVER

ATELACTASIS

ATELACTASIS OR PNEUMONITIS Anesthesia agents cause increase production

of secretions, as water evaporates, they become viscous.with diminished cough reflex & decrease ciliary activity - formation of mucus plug- obstruct small airways. When the gases distal to plug get absorbed the airways collapse.

Febrile response is due to Low grade infection distal to obstructing plug and absorption of bacterial pyrogens

Temp elevation within 12 hrs of onset of plug formation.max temp is characteristically 38.9 degree centigrade

PNEUMONITIS

High risk group - Cigarette smoking, chronic bronchitis, COPD

3% of all ORS, 15% abdomen, 25% upper abdomen

Continued atelactasis predispose to full blown Pneumonitis

Prevention: Assessment of patient, Avoid General Anaesthesia,

Stop smoking, spirometery, Assess pulmonary mechanics, Thick mucus secretions need inhalations to FOB, chest physiotherapy, early mobilization.

THIRD DAYSURGICAL FEVER48-72HRSTEMP ELEVATION TO 40.6 TO 41.1

Phlebitis

PHLEBITIS

IV catheter sepsis DVT and Pulmonary embolism Suppurative thrombophlebitis

Temp elevation to 40.6-41. 1°C Tachycardia, Hypotension, Oliguria, Prostration,

Leukocytosis, Hard chills-52%develop septic shock, mortality rate 40% in 40yrs above age and 80% in above 80yrs age.

Tenderness and erythema around catheter.

Precipitating causes: Hyperosmolar infusate, K conc sols, antibiotics,

size of vein in which catheter. This can be decreased by adding one unit of heparin. IV septic technique

Cathater sepsis reduced from 23% to 4% keeping Intravenous catheter in place for max 12 hrs.

IV catheter sepsis

Lack of aseptic technique Use of hypertonic solutions Multiple infusions through same line Change of site after 72 hrs. Early signs-Red streaks

THIRD AND FOURTH DAY FEVER

DVT & PULMONARY EMBOLISM

DVT & PUL. EMBOLISM

3 -4 days Temp elevation, calf Tenderness (Homan’s sign)

Doppler ultrasound, has replaces contrast venograms

Treatment is PREVENTION Identify High risk group from pre-op

stage. Start prophylactic heparin sub cut peri-

operative Mechanical means

PULMONARY EMBOLISM

SEQUELAE OF DVT

FEVER DOES NOT APPEAR UNTIL PUL THROMBO EMBOLISATION-PAIN CHEST, DYSPNOEA,

TREATMENT IS PREVENTION

THERAPEUTIC DOSE OF HEPARIN

NEED HDU

SUPPURATIVE THROMBOPHLEBITIS PRESENCE OF SUPPURATIVE

INFECTION IN VEIN IS OFTEN LETHAL-NEED LIGATION OF VEIN

HIGH FEVER , REMITTENT TYPE

COMMON SITES ARE; Basilic,Cephalic, Neck veins

OCCASIONALLY SEEN IN PELVIC VEINS after SEPTIC ABORTION, AND PID.

URINARY TRACT INFECTIONS

Most common nosocomial infection (40%) 75% patients have some form of urine tract

manipulation Bacteria found in urine in 1-5% of patients

undergoing short term catheterization, 90% pts in whom Foley is left for 48hrs or more

Post op UTI; temp 39.4-40°C, rigors/chills Management –prevention, PUT Catheter only when

must, Aseptic technique , closed drainage system. Discard drainage system if accidentally disconnected and change when obstruction or contamination occurs.

DAY 5-8 FEVERSurgical wound infection

SURGICAL INFECTION

Wound infection‘ present as abscess-cellulites

Signs of erythema, foul discharge, indurations, soakage

Treatment is adequate drainage &/antibiotic coverage

Factors responsible-patient related , disease related, procedure related, environment related.

Lack of preventive measures.

BENIGN POST OPERATIVE FEVER

During Operation Thermo regulatory mechanism Hypothalamus becomes inhibited by Anesthetic agents –fall in body temp, thermo neutrality with atmosphere

Once anesthesia effect is gone- recovery of this mechanism but intracranial core temp still decreased-thermosenstive receptors in hypothalamus sense decreased temp and attempt to raise body temp to hypothalic set point, often there is over compensation with a mild febrile episode in post op period

This is diagnosed by exclusion

Other non surgical Causes….. MALARIA, BRUCELLA, TYPHOID.

MALIGNANT DISEASES

POST CARDIOTOMY FEVER SYNDROME

BLOOD TRANSFUSION

PHAYNGITIS - OTITIS

ADDISONIAN CRISIS

OTHER CAUSES

Hyper metabolism -increased BMR in response to surgery –burn pt, returns to normal with wound healing

Drug induced Fever

DEHYDRATION-decreased sensitivity to sweating mechanism

Malignant Hyperthermia

THYROID STORM

FEVER OF CNS ORIGIN

DRUG INDUCED FEVER

Drugs that cause fever due to effects of pharmacological activity; Antibiotics, Cytotoxic agents

Drugs causing fever due altered thermoregulation Atropine, Catacholamines, (Decrease sweating) Increased BMR- thyroxine derivatives

Drugs causing fever due to contaminants; IV solutions

Drugs that cause fever indirectly; anticoagulants

Drugs causing fever due to hypersensitivity-sulphas, penicillins,

MANAGEMENT OF POST OP FEVER Measures/procedures to determine cause

History;onset,type, medication-blood transfusion Exam;chest, IV sites, lower limbs DVT, calf tenderness,

ENT exam, assess Hydration,

Lab work. CBC, urine routine/cs, Chest X-Ray, C/s-Throat, nasopharynx, wound, blood culture

( x2 )if temp >38.9

Culture; Drain or tube, or cath tips, iv caths Typhoid, Brucella-tests. Treat; underlying cause. Treat fever, maintain

hydration, nutrition

SUMMARY

Fever is common and readily detectable manifestation of disease .In the post op pt the most common potentially serious causes are atelactasis or other pulmonary problems, phlebitis in deep veins or at iv sites, UTI, and surgical wound infection.

Other benign and potentially serious causes occur less commonly but must be suspected when more common causes are not found. treatment directed towards cause. Fever controlled by salicylates and by mechanical means if control is warranted,