Comorbidities associated with delayed resolution of pneumonia

1. COPD
Impaired cough and mucociliary clearance
2. Alcoholism
Aspiration, malnutrition, impaired neutrophil function
3. Neurologic disease
Aspiration, impaired clearance of secretions and cough
4. Heart Failure
Edema fluid, impaired lymphatic drainage
5. Chronic Kidney disease
hypocomlementaemia, impaired macrophage and neutrophil function, reduced humoral immunity
6. Malignancy
Impaired immune function, altered colonization, effects of chemotherapy
7. HIV
Impaired cell mediated and humoral immunity
8. Diabetes Mellitus
Impaired neutrophil function and cell mediated immunity

Clinical Approach to the Septic Patient

Diagnosis For both community and hospitalised patients presenting with sepsis:

1. Diagnose or rule out mimics of sepsis by history, physical examination and routine lab tests


2. Initiate medical therapy appropriate for disorders mimicking sepsis


3. If mimics of sepsis are ruled out determine site of septic focus in critically ill patients presenting with sepsis, distinguish colonisation from infection in isolates from urine, respiratory secretions and noninfected wounds


4. Treat infection and avoid treating colonizing organisms

Interventions

A. Antibiotic interventions

i. Select empiric monotherapy based on coverage of predictable pathogens determined by focus of infection

ii. Select antibiotic with low resistance potential

iii. Select antibiotic witn a good safety profile

B. Non antibiotic interventions

i. Administer aggressive and effective intravascular volume replacement

ii. If pressors are needed, give volume replacement before pressors

iii. Restore normothermia with heating blanket

iv. Surgical intervention if sepsis is related to intra-abdominal organ perforation or obstruction or abscess. For infected devices, remove the device.

It is of paramount important to give fluid therapy before giving vasopressors. If the hypovolemia is not corrected promptly the patient will progress to a refractory shock state. By then the tissue perfusion would not respond to vasopressor drugs, even the blood pressure and intravascular volume were to be restored and cardiac output would remain depressed. The resultant lactic acidosis further depresses the myocardium and worsens the hypotension. The common complications of prolonged shock are massive bleeding, DIC and MODS which are often fatal.

Questions:

1. List the likely pathogens in gram negative sepsis in a patient who has been on meropenem for a week?

a. stenotrophomonas

b. MDR acinetobacter or pseudomonas

2. List the factors which result in failure in resolution of sepsis despite antibiotic therapy

• 
  
  wrong antibiotic choice


• 
  
  delayed administration of antibiotics


• 
  
  Inadequate source control


• 
  
  Inadequate antimicrobial blood levels


• 
  
  Inadequate penetration of the antimicrobial to the targer site


• 
  
  antimicrobial neutralization or antagonism


• 
  
  superinfection or unsuspected secondary bacterial infection


• 
  
  nonbacterial infection


• 
  
  noninfectious source of illness

pseudosepsis

Within last two weeks, I have diagnosed and treated 3 H1N1 pneumonia with ARDS. One who is severely obese (BMI>60), one pregnant lady who just had LSCS due to fetal distress and then a student who presented as acute exacerbation of bronchial asthma eventhough the last attack was more than 15 years ago. I used fluid restriction strategy with frusemide to keep even balance, according to FACTT trial and ARDS net ventilation strategy but with initial PEEP of 14-16cmH2O.
I have noticed in one patient, the WCC rised to more than 30,000 but her cultures were all negative. Anyway, I'd changed all of her lines. Her condition was alway stable with only low grade fever.
----------------
Pseudosepsis
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Conditions that mimic sepsis
Common disorders:
1. Diuretic induced hypovolemia
2. Acute GI hemorrhage
3. Acute PE
4. Acute MI
5. Acute (oedematous/necrotic) pancreatitis

Uncommon disorders:
1. Diabetic ketoacidosis
2. SLE flare
3. Relative adrenal insufficiency
4. Rectus sheath hematoma

Several conditions may present with acute abdominal pain accompanied by fever, leukocytosis with a left shift and hypotension mimicking intra-abdominal sepsis. Such patients may have SG catheter readings that are compatible with sepsis. These medical disorders include diabetic crisis in diabetic ketoacidosis, luetic crisis in patient with syphilis, right rectus syndrome in patients with EBV infectious mononucleosis, rectus sheath hematoma, acute porphyria, SLE flare involving the peritoneum, acalculous cholecystitis due to vasculitis, dissecting AAA, splenic rupture, and pseudoappendicitis due to yersinis enterocolitica or other organism. These medical mimics of acute intra abdominal sepsis are serious disorders, many of which have specific treatments.
The correct presumptive diagnosis is essential for effective therapy of sepsis as well as in the disorders mimicking sepsis.

Anion Gap

Approach to ABG analysis, the principles

1. Check arterial pH for net deviation
2. Assess the pattern
3. Look for associated clues
4. Assess the compensatory response
5. Check for additional indices for metabolic acidoses

If the patient has metabolic acidosis, determine whether it is normal anion gap or high anion gap metabolic acisosis. Correct the anion gap to patient's albumin level.
Look for mixed disorders e.g. mixed normal with HAG acidoses.
Important gap and other indices in ICU

1. Anion gap
2. Osmolar gap
3. Delta gap
4. Delta ratio
5. Lactate gap
6. Oxygen saturation gap
7. Urinary anion gap

Pearls and nonsense

• The absence of an anion gap does not exclude typical causes of anion gap acidosis, i.e. DKA may present without an anion gap.
• There is no identifiable cause of an HAG in 1/3 of patients.
• Large AG are most commonly DKA or lactic acidosis, less commonly ethylene glycol. Higher AGs correlate with increased severity of illness.
• Delta gap of > 2 - the presence of a mixed disorder is likely.

A reduced anion gap may be seen with :
-->Principle: decreased unmeasured anions, increased unmeasured cations and analytical errors.

• hypermagnesaemia
• hypercalcaemia
• Lithium toxicity
• Excess Immunoglobulins (multiple myeloma, intragam infusion)
• hypoalbuminaemia

Causes of elevated AG without acidosis:

• dehydration
• alkalosis
• sodium salts of unmeasured anions (citrate, lactate or acetate)
• certain antibiotics ( Na penicillin, carbenicillin)
• decreased in unmeasured cations (severe combined hypomagnesaemia, hypocalcaemia and hypokalaemia)

Define standard base excess (SBE): ?
ANION GAP: Anion gap is 'unmeasured anions, = (Na + K) - (Cl + HCO3)
Metabolic acidosis (reduced bicarb) must be associated with either an increased of the AG (HAG acidosis) or of the Chloride (NAG or hyperchloraemic) since the overall quantity of cations and anions must match bicarb loss from gut or kidney.With replacement by Cl- containing fluid will result in a non anion gap hyperchloraemic acidosis.