SIR WILLIAM OSLER

“HUMANITY HAS BUT THREEGREAT ENEMIES: FEVER,FAMINE AND WAR; OF THESEBY FAR THE GREATEST, BY FARTHE MOST TERRIBLE, ISFEVER.”

Tc 37.5 °C

• subfebrility

Tc < 40 °C

• fever

Tc > 40 °C

• hyperpyrexia

External and internal factors affectingfever

• Cold environment: pyrogens might inducehypothermia rather than fever

• Hypoxia: decreased pyrogen effect

• Newborn, old patients: hypothermia is more frequent

• Less fever in those fasting

►There is no association between the extent of

fever and severity of illness

The biological value of fever

• metabolic changes: synthesis of acute phaseproteins

• high temp is associated with decreased serum ironlevels: decreased bacterial growth

• high temp might be bacteriostatic, even bactericid

• augmentation of cytokine effects: 5-6 x increase inactivity @ 39 °C vs. @ 37 °C

• increased cellular and humoral immunity

Unfavourable effects of fever

• heat-stroke like high temp (rare)

• febrile convulsions (from 6 months to 6 yrs, above 39°C -14%)

• cerebral metabolic derangement: delirium, hallucinations

• cardiac patients, elderly: increased CO, decompensation

• increased minute ventilation: increased work of breathing

• prolonged febrile states: anorexia + increased core temp

• diabetics: some cytokines have antiinsulin effects

• early pregnancy: teratogenesis?

• too high temp inhibits immune functions

HYPOTENSION

AGE

HEADACHE

PETECHIAE

LOW BACK PAIN

AMS IVDA TRAVEL (CONTACT) TC > 41⁰C, DURATION

IMMUNSPURESSION / ASPLENIA

NIGHT SWEATS, WEIGHT LOSS

ALONG WITH ANTIBIOTICS

FOLLOWING HOSPITALIZATION(NOSOCOMIAL) LARGE NUMBER OF PATIENTS WITH SAME SYMPTOMS(BIOTERROR)

> 40-41°C

EXTERNALHEAT CHALLENGES

INTERNALHEAT CHALLENGES

DRUGS

SUSCEPTIBLE DISEASE

OTHERS

ENVIRONMENTRAL HEAT; RADIATING HEAT, HUMIDITY

INCREASED PHYSICAL ACTIVITY

DRUGS INHIBITING SWEATING (ANTICHOLINERG, ANTIHYSTAMIN)COMPOUND INCREASING METAB. RATE (COCAIN, LSD, AMPHETAMINE)DIURETICS; ALCOHOL

EXSICCOSIS; SKIN (BURNS; FIBROSIS; SCLERODERMA); OBESITY; INCREASED METAB. RATE-ACTIVITY (PARKINSON, HYPERTHYREOIDISM, PHEOCHROMOCYTOMA)

INABILITY TO ADAPT; PREVIOUS HEAT STROKE;INSOMNIA; INFECTION; EXTREMES OF AGE; CLOTHING

HYPERTHERMIA

NMSANTICHOL

SYMH

HEATSTROKE

SER.SY

D2 Ca (ICP)ANTICHOL

GABA5HT

EP-RIGID CONTR FLACCID NORM. INCREASED

+++ +++ -- --- +

Fever and toxins

PHYSOTIGMIN (*)

MYDRIASIS BLURRED VISION FEVER DRY SKIN FLUSHING ILEUS URINARY RET. TACHYCARDIA HYPERTENSION PSYCHOSIS COMA SEIZURESMYOCLONUS

ANTIHYSTAMINEATROPINBACLOFENTCAD*PHENOTHIAZINESCOPALAMINE

IRRITABILITY HYPERREFLEXIA FLUSHING DIARRHEA DIAPHORESIS FEVER TRISMUS TREMORMYOCLONUS

FLUOXETINEMEPERIDENIEPAROXETINESERTRALTINETRAZODONECLOMIPRAMINE

BENZODIAZEPINE

FEVER

MUSCLE RIGIDITY

AUTONOMIC DYSFUNCTION

ALTERED MENTAL STATE

HYPOTHALAMUS

NIGRO-STRIATUM

MEDULLA OBL.

MESOCORTEX

CENTRAL DOPAMINERGIC (D2) DYSFUNCTION

PARKINSONIAN HYPERPYREXIAN SYNDROME

NEUROLEPTIC MALIGNANT SYNDROME

OCCURS IN 0,1-0,2 % IN PTS TAKING NEUROLEPTIC MEDS

AFFECTS MAINLY YOUNG MALE PTS (< 40 YRS)

HIGH MORTALITY(50-70%)

NEUROLEPTICS

CYCL. ANTIDEPRESSANTS

MAO INHIBITORS

ANTIEMETICS

LITHIUM / ECT

Heat exhaustionand heat stroke

HOT, SWEATY SKINPROFUSE SWEATING DIZZINESSSEVERE WEAKNESS NAUSEA, VOMITING TACHYCARDIA OLIGURIA (CONC. URINE)AMS

HOT, DRY SKIN Tc> 40°C AMS - OBS TACHYCARDIA TACHYPNOEMUSCLE SPASMS

HEAT EXHAUSTION HEAT STROKE

> 40-41°C

OXYGENVOLUME EXPANSION

PYROGEN?• INFECTION• INFLAMMATION• NEOPLASM

HEAT STROKE?• ENVIRONMENT• INCREASED ACTIVITY• HYPOVOLEMIA

DRUGS?• MH• MNS*• ANTICHOLINERGICS• ANTISEROTONERGICS

STOP MEDSACTIVE COOLINGMUSCLE RELAX.DANTROLEN

0.8-1.5 mg/kg/6hAMANTADIN*BROMOCRIPTIN*

ACTIVE COOLING

• ISOLATION• SURFACE• INTERNAL• PHARMACEUTICAL

Symptoms Possible Cause Action to Take

Intense pain in the lower right side of the abdomen. Slight fever.

Appendicitis Go to an emergency room now

Severe pain in the upper abdomen and often spreads to the sides and the back. Nausea, vomiting, fever, …

Pancreatitis Call 911 or go to an emergency room right away.

In a woman: dull, constant pain in the lower abdomen along with vaginal discharge and fever.

Pelvic inflammatory disease. See a doctor promptly.

Pain and feverA few examples

Abdominal pain

Environmentalinteractions

Pain behaviour

Suffering

Pain perception

Nociception

The multi-dimensional approach of pain

Bio-Psycg-Social Model

General considerations

• Accounts for 10 % of ED visits

• Can be associated with simple problemsbut also with serious conditions

• 1/3 of cases are UDAP

Types of abdominal pain

• Visceral– caused by distension, ischaemia of hollow organs– colicky, crampy pain

• Parietal– caused by inflammation, ischaemia or distension of the

parietal peritoneum– more circumscribed,provoked by cough, movement– guarding is due to this type of pain

• Referred– radiates to distant locations from the affected organs– afferent fibers from different locations travel together– e.g. AMI – epigastrial pain

ruptured aortic aneurysm traumamesenterial ischaemia ileus ACS visceral perforation visceral rupture

Physical examination

• Palpation and auscultation

• Cough test: pt holds hands over affected area

• Heel drop test

• Murphy-sign: palpating RUQ inspiration stops

• Psoas-test: pt flexes hips against resistance

• Obturator-test: hip is rotated in and out

• Rovsing-jel: palpating LLQ provokes pain inRUQ

Imaging(US, X-ray, CT)

• FAST

• abdo US by radiologists

• X-ray

– plain: free air, niveaus, distension

• CT

– highly informative, can be plain or contrastenhanced

Bloods, biomarkers

• FBC

• LFTs

• amylase, lipase

• serum lactate and lactate clearence

RANSON SCORE

Disposition

• One can not always clarify the exactpathophysiology of abdo pain in the ED.

• Primary goal is to recognize critical and emergent conditions, start painmanagement, stabilization and start diagnostic procedures

• Abdominal pain management is team-work!

SEPSIS

SIRS2 OR MORE

36°C < T < 38°CBPM > 90/minRR > 20/MIN (PaCO2 < 32 Hgmm)4 > WBC > 12 / 10% ÉRETLEN ALAK

SEPSIS1 OR MORE

SIRS + DOCUMENTED INFECTIONALTERED MENTAL STATEHYPOXAEMIA (FiO2 = .21 paO2 < 72 Hgmm)se.LACTAT EOLIGURIA (UOP < 0.5 ml/kg/h)

SEVERE SEPSIS SEPSIS + ORGAN FAILUREHYPOPERFUSION

SEPTIC SHOCK SEPSIS (INDUCED)SBP < 90 HgmmMAP < 60 HgmmDIFFERENT FROM USUAL BP (-40 Hgmm) VOLUME REFRACTER

2012

2011

2010

2009

2008

2007

2006

2005

20042003

2002

The Barcelona Declaration

SSC GUIDELINES 2004

SSC GUIDELINES 2008

SSC GUIDELINES 2012

2013.

0 20 40 60

HALÁLOZÁS (%)

SEPTIC SHOCK

SEVERE SEPSIS

SEPSISMORTALITY (%)

ORGANISMSYSTEMIC INFLAMMATION OR

INFLAMMATORY RESPONSE

SEVERE SEPSISGLOBAL TISSUE HYPOXIA

AND ORGAN DYSFUNCTION

DIFFUSE ENDOTHELIAL DISRUPTION AND MICROCIRCULATION DEFECTS

MOD AND REFRACTORY HYPOTENSIONSEPTIC SHOCK

Nguyen H.B. – Ann Emerg Med 2006; 48:28-54

TLR-Toll-like receptor, CLR-C-type lectin receptor, NLR- nucleotid binding oligomerization (NOD) receptors

What to do?

New England Journal of Medicine, 2001; 345(19), 1368–1377.

33%

2006.

SEPSISRESUSCITATION

BUNDLES

SEPSISMANAGEMENT

BUNDLES

EARLYRECOGNITION

TRIAGE

CHAIN OF SURVIVAL IN SEPSIS

TRIAGE

EARLY RECOGNITION

CHAIN OF SURVIVAL IN SEPSIS

GENETIC VARIABILITYE.G.DIFFERENT CYTOKINE

RESPONSE

INTRINSIC FACTORSAGE

COMORBID STATEIMMUNSUPRESSION

NUTRITIONGATES OF INFECTION

SURGICALINCISION

STERILE vs CONTAMINATEDACUTE vs ELECTIVE

IMPLANT

EXTRINSIC FACTORSENVIRONMENT

WORKCONTACT

EXPOSITION

HOSPITAL FACTORSDURATION OF HOSPITALISATIONLOCATION OF HOSPITALISATION

LOCAL INFECTIVE AGENTSMEDICATION

INTERVENTIONSVENOUS CANULAE

URINARY CATHETERWOUND - DECUBITUS

TRIAGE

P REDISPOSITION

I NFECTION

R ESPONSE

O RGAN DYFUNCTION

TRIAGE

SBAR COMMUNICATION

SITUATION

B ACKROUND

A SSESMENT

RECOMMENDATION

SITUATION SUSPICION OF SEVERE SEPSISBACKGROUND SIRSSUSPICION OF INFECTION PERFUSISON DEFECT (ORGAN MANIFSTATION)ASSESSMENTTRIAGE (EVALUATION OF VITALS AND SpO2)

TRIAGERECOMMENDATION DECISION ± HELP ABG-LACTATE-FBC SAMPLING (MICRO+LAB) HYPOPERFUSION– HYPOTENSION: IV-LINE (SALINE 20ml/kg IV )

SEPSIS TEAM

2013

2013

2013

2013

0

10

20

30

40

50

60

70

1 2 3 4 5 6 7

CHANCE OF SURVIVAL (%)

EVERY HOUR DELAY IN GIVING ANTIBIOTICS IN SEPTIC SHOCK DECREASES THE CHACE OF SURVIVAL BY 7.6%!!

(DELLINGER- 2004; KUMAR – 2006)

ANTIBIOTICS

(< 3 HRS / < 1 HR)

2013

2013

2013

2013

Do not missdiagnoses!

DEXAMETHASON 1mg (before AB!)CEFTRIAXON 2gVANCOMYCIN 10-15mg/bw kgAMPICILLIN 3gACYCLOVIR 10mg/ttkg

MENINGITIS ENCEPHALITIS

MENINGOCOCCAEMIA

MORTALITY > 70%

CEFTRIAXON - 2G

STEROID (DEXAMETHASON) – 10MG

TOXIC SHOCK SYNDROME

HIGH FEVERSHOCKERYTHRODERMAMUC.MEMBR. HYPERAEMIAMYALGIAPHARYNGITISDIARRHOEA

EXTREME PAINNECROTISING FASCIITIS

MORTALITY 30 - 80%→ FACIITIS (70%) 60%→ MYOSITIS 85-100%

PENICILLIN - 10MECLINDAMYCIN – 900MG

IMMUNGLOBULINSURGICAL DRAINAGE

RESUSCITATIVE BUNDLE

TOXIC SHOCK SYNDROME