Infection - The febrile patient - Sepsis

Causes

Precipitating - microbiological agents

• Bacteria, Viral
• Rickettsia, Mycobacteria
• Fungal
• Protozoan
• Parasite
• Prion

Predisposing

Congenital

• Primary immunodeficiency

Acquired

• Breach of anatomical defences
• Chemotherapeutics - cancer patients
• Immunosuppressants - transplants patients
• Immunomodulators - rheumatological and renal patients
• HIV

Organism related

• Various mechanisms that evade immune defences e.g. gram negative, mycobacteria, retroviruses
• Various mechanisms that defeat antimicrobials e.g. altered receptor sites, enzymatic neutralisation

Perpetuating

• Abscess
• Collection
• Foreign body - joint replacements, vascular grafts, various stents, IUD, implantable devices
• Poor nutrition
• Poor blood supply

Course

• Acute
  Chronic

Complications

• Bacteraemia (or viraemia, fungaemia etc)
• Systemic inflammatory response syndrome
• Septic shock (high mortality)

Common sites of bacterial infection

• Cardiac - endocarditis
• Upper respiratory - tonsillitis, otitis media, otitis externa
• Lower respiratory - pneumonia, bronchitis
  GI Tract - gastroenteritis, hepatic abscess, appendicitis, diverticulitis, perianal and related abscesses
• GUS - cystitis, pyelonephritis, epididymo-orchitis, PID
• CNS - meningitis
• Skin - cellulitis
• Bone - osteomyelitis, septic arthritis

Commons sites of viral infection

• Cardiac - pericarditis, myocarditis
• Upper respiratory - laryngitis, pharyngitis
• Lower respiratory - pneumonia, bronchitis
• GI system - gastroenteritis, hepatitis
• CNS - Encephalitis
• Skin - herpes zoster/simplex

SEPTIC SHOCK

Pathogenesis

• Bacterial components causing systemic inflammatory response and circulatory failure (^ temp, ^ WCC and inflammatory markers) *

Pathophysiology

• Vasodilation - warm peripheries, bounding pulse (later cold and poor pulse when circulation failing) >> DISTRIBUTIVE SHOCK
• ^ vascular permeability - v circulating blood volume > Hypovolaemic shock
• Direct myocardial depression (later) - v contractility > Cardiogenic shock

• Shock > Anaerobic metabolism > Metabolic acidosis (v pH, v bicarb) , ^ lactate

Compensatory mechanism

• Sympathetic response - ^ HR, contractility, vasoconstriction (to overcome 'vasoplegic' state)

Mortality rate (varies depending on source of infection and severity)

• ~ 30%

Treatment principles

Fluid resuscitation and circulatory support

• Fluid resuscitation vital signs and urine output normalise or evidence of fluid overload/pulmonary oedema (alternatively MAP 70, CVP 12 cmH2O / PAWP 15cmH2O )
• Vasopressors if above fails and systemic vascular resistance remains low
• Inotropes if above fails and cardiac index remains low

Early and appropriately dosed antibiotics

• Attempt to obtain microbiological specimens rapidly (e.g. blood culture, urine culture etc)
• Give antibiotics within 1 hour of diagnosis (do not delay if specimens cannot be obtained)
• Broad spectrum antbiotics if source unidentified

Early and aggressive surgical debridement or drainage if indicated