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Transcript
Management of fever on the ward/ PUO M Armstrong THE CASE Mr. H, 67 year old Day 6 post R TKJR PMH: DM2 HTN OA- Previous L THJR You are the ward call and the treating team have gone home. Mr. H, spikes a fever to 38.7 You are called by the nurse. What will you do? What would you do? ABCD On review: RR 28, sats 93% on 2L NP (pre-op 96%ra), T38.2, HR 105, BP 102/60 (pre-op noted to be 140/82) • What could be causing his fever? What are the main causes of fever in hospitalized patients post surgery, i.e. in this patient? • How would you like to investigate him and manage him? Fever • A common symptom • In top 10 general practice presentations • 5% of ED presentations • Many reasons to have fever while in hospital - Infection is the most common cause of fever of short duration Definition “an elevation in core body temperature above the daily range for an individual” UTD Normal temperature varies over the course of the day (low ~6am, high ~4-6pm with variation ~0.5), control is via the thermoregulatory center in the anterior hypothalamus No clear consensus of what actually constitutes a fever but UTD defines morning reading over 37.2 and evening over 37.7 as greater then 99th percentile for healthy subjects (based on ‘92 study of 700 oral temperature readings *tympanic likely to be higher) Older patients likely have a lower set point and may have lower fevers with more severe fevers (immunosuppression is less well defined, but likely that febrile response is blunted) Pathophysiology Increased “set-point” from hypothalamus in response to infection/ inflammation. Elevated prostaglandin E2 mediated (hence how an antipyretics work) -activates neurons in vasomotor centre> vasoconstriction, increased peripheral heat production and liver/ fat thermogenesis “chills and rigours” PYROGENS “any substance that causes fevers” Exogenous -microbes and their toxins (e.g. LPS, TSST-1) Endogenous (pyrogenic cytokines) -specific cytokines produced on activation of TLR -cytokines are proteins that regulate immune, inflammatory and hematopoietic processes -IL-1, IL-6, TNF, IFN-alpha All end up increasing production of PGE2 Assessment • Usually follows a fairly uniform course with some modifications according to the severity of patient status, epidemiologic factors, and the patients background • Fever without with-out an initial obvious source is not PUO but “fever without localizing signs” UTD “most febrile illnesses either resolve before a diagnosis can be made or develop distinguishing characteristics that lead to a diagnosis” Assessment- history/ exam • Important as 85% of adults with several days fever will have localizing symptoms/ signs • Of patients with no localizing signs, more then a 3rd still have bacterial infection (think LRTI/ UTI) History/ exam • Just like the usual… -But Methodical approach Review vitals and trend Look for signs associated with localized symptoms Beware of hidden areas/ traps (remove covers, think teeth, temporal arteries, sinuses , thyroid, axillae, joint flexures, natal clefts, perineum, prostrate, genitalia Reassessment over time and 2nd opinions can be important Warning signs • Beware of potentially severe infection -A short time frame of fever to presentation (<12 hours) -Incapacitated (“bedbound” “never been this sick”) -Pallor, mottled skin, cold peripherals -Severe muscle and joint pain (in in absence of significant fever) Concerning vitals • Tachypnoea [>30] -often overlooked but a strong predictor or severity of disease (and an early sign) • Tachycardia [>120] -over 120 is unusual and portends septic shock • Hypotension [<100] -regard as septic shock until proven otherwise, do not assume only 2nd dehydration, be aware of patients baseline blood pressure Concerning vitals • Temperature [>39] -Don’t forget “cold sepsis” and trends -Over 39 in adults likely to be from a significant infection Features that can suggest bacterial infection • Rigors (can be confusing in history taking) -if true rigor suspect bacterial infection until proved otherwise (admit, investigate) • Altered LOC/ behaviour change -CNS infection or systemic, can be subtle (ask family) • Repeated vomiting in absence of diarrhoea -can be a sign of bacteraemia, intra-abdominal pathology or CNS pathology. Investigations • Be guided by localizing features and clinical circumstances -FBC -Blood cultures -CXR -Urine microscopy and culture -LP -CRP/ESR -Nose/Throat swabs for PCR tests Initial Management • Infections requiring urgent treatment or concerning vitals/ signs -Broad-spectrum empiric antibiotics SIRS criteria and sepsis http://nrsged.wikispaces.com/6.+SIRS+vs+Sepsis Back to the case… radiopaedia.org PUO • Classic definition (Petersdoft and Beeson 1961) -an illness of at least 3 weeks’ duration -a fever above 38.3 on several occasions -no diagnosis reached after one week of intelligent and intensive investigation Further separated into 4 categories 1. 2. 3. 4. “Classical” PUO PUO in hospitalized patients (nosocomial) PUO in HIV-infected patients PUO in neutropenic patients Establishing that a patient has PUO The following evaluation should be unrevealing: 1. History 2. Physical examination 3. Complete blood count, including differential and platelet count 4. Blood cultures (before antibiotics, 3 sets drawn from different sites with an interval at least several hours between sets) 5. Routine blood chemistry including LFT’s and bilirubin 6. HAV, HBV, HCV if LFT’s abnormal 7. Urine analysis and culture 8. CXR If any symptoms or signs suggest specific organ involvement then further targeted investigation has been unrevealing Changing epidemiology Since 1950’s fraction of PUO’s undiagnosed has been increasing Early PUO series included few connective tissue disease, which are now better characterized Extra-pulmonary TB, solid tumors, intra-abdominal abscesses are now easier to diagnose Infective endocarditis is now easier to diagnosis and there are less cases of “culture negative” endocarditis due to better culture techniques (although in the current era more PUO are culture negative IE or IE due to difficult to isolate organisms) Causes of PUO * (Table from Infectious Diseases: A clinical approach, Yung et al) Infection (15-25%) Neoplasm (<20%) Inflammatory disorders (15-25%) Miscellaneous Systemic: Bacterial- TB*, salmonellosis, brucellosis, psittacosis, meliodosis Viral- CMV, EBV, HIV Other: Q fever, malaria, amoebiasis, toxoplasmosis Localised: With abscess formation* -in/around kidney -in/around liver -around colon -in pelvis -in/ around spleen -dental Without abscess formation -endocarditis -osteomyelitis -cholangitis -pericarditis Lymphomas and lleukaemia Solid tumours: kidney, lung, liver, gastric, atrial myxoma, disseminated carcinoma Giant cell arteritis PMR Adutl onset Still’s disease SLE Granulomatous disease (Crohn’s, sarcoidosis, granulomatous hapatitis) PAN Other vasculitides Drug fever (rash in only 25%) VTE Haematoma Endocrine disorders (subacute thyroiditis, Addison’s disease, hyperthyroidism, pheochromocytoma) EtOH hepatitis and cirrhosis Chronic aortic dissection Factitious fever Others *The most common infective causes in many studies *9-51% remain undiagnosed PUO in sub-populations Age- older age groups more likely to get auto-immune multisystem disease HIV/AIDS- need to take into account immunosuppression (CD4 count and viral load) -need to think of mycobacteria (MAC) and lymphomas Neutropenia- most often linked to bacteraemia. Fungal infections replace bacteria infections in prominence after the acute period (7 days). Fever is often confounded by sick patients with multiple possible causes of fever including the underlying diagnosis POSTOPERATIVE FEVER -fever above 38 common in first few days secondary surgical trauma Need to think of timing and type of surgery: Immediate- onset in theatre or within hours of surgery Acute- onset within first week of surgery Subacute- onset from one to four weeks post surgery Delayed- onset more then one month after surgery Immediate: -drugs or blood products in the peri-operative period -trauma (prior or as part of surgery) -infections present prior to surgery -malignant hyperthermia *fever due to trauma of surgery usually resolves in 2-3 days Acute: -nosocomial infections (SSI, catheter related infection) -pneumonia (including VAP, aspiration) -UTI (including CAUTI) Non infectious causes- MI, VTE, Pancreatitis, EtOH withdraw, acute gout Subacute: -SSI (more common then in the acute period) -catheter related in infection -C. dif -drug fevers -thrombophlebitis -VTE Delayed: most delayed fevers are due to infection -SSI due to more indolent organisms (eg, Coagulase negative staph in PJI) -cellulitis (disrupted venous/ lymphatics) -infective endocarditis (perioperative bacteraemia) -viral/ parasitic infections from blood products What about atelectasis? Concurrence probably coincidental rather causal UTD- “there was no association between fever and the presence of, or the degree of, atelectasis” “Wind, Water, Wound, What did we do?” Drug fever: -Antimicrobials (sulfonamides, penicillins, vancomycin, nitrofurantoin, antimalarials) -H1 and H2 antagonists -Anti-epileptics -NSAIDs -Anti-HTN (hydralazine, methyldopa) -Antiarrhymic drugs (quinidine, procainamide) -Antithyroid drugs -Digoxin and aminoglycosides (rare) “Fever of unknown origin is more often caused by an atypical presentation of a common entity than by a rare disorder” Clinical approach- HX -A thorough history often repeated 1. Verify presence of fever, continuous/ intermittent 2. Establish onset/ duration 3. Seek localising symptoms 4. Establish severity 5. Obtain co-lateral information (family, GP) 6. Consider past history for clues 7. Ask about medications, including OTC, SCAM, immunosuppression, antimicrobials, allergies 8. Ask about country of birth, travel, occupation, animal contacts 9. Sexual history/ IVDU Clinical approach- Ex Think head to toe “check list” -eyes (scleritis, uveitis, conjunctival haemorrhage) -Optic fundi -temporal arteries -sinuses -? Change in behaviour/ cognition -oral cavity (teeth and gums) -thyroid -hands -heart- new murmurs/ rub (listen carefully to the heart for rubs/ new murmurs) -lymph nodes -sternum ? Bone tenderness -abdominal organs- ? organomegaly -blood vessels/ rash- ? vasculitis -rectal/ pelvic exam -genitalia -lower limbs- ? DVT Clinical approach- IX • Initial approach as for any fever - Other early tests may include ANA, RF, HIV, EBV serology, CMV serology, CRP/ESR, LDH, CK - If no leads from above consider stool specimen for MCS, Q fever, brucellosis, leptospirosis, syphilis, psittacosis, toxoplasmosis, TB screening, anti-ENA, ANCA, dsDNA, SPEP, cryoglobulins, Ix- imaging • • • • • • CT CAP or more specific CT scans US of abdomen/ pelvis MRI ECHO Doppler US legs (VTE) Nuclear med scans (gallium labelled leukocyte scan) • PET scans Ix- invasive tests • Lumbar puncture • Tissue biopsies- lymph nodes, skin, renal, muscle, bone biopsies, temporal artery biopsy, bone marrow, liver -remember to send for culture (including mycobacterial and fungal) and not just histology! “Most adults who remain undiagnosed after an extensive evaluation have a good prognosis”