Question

Lisa has a urinalysis which reveals pyuria and microscopic hematuria. A complete blood count (CBC) reveals leukocytosis and she has an elevated C-reactive protein. Her complete metabolic profile (CMP) reveals acutely altered electrolyte balances.

Lisa’s temperature is 101.2, and her blood pressure is low (82/45). She is diagnosed with sepsis due to pyelonephritis and transferred to the intensive care unit.

• Define pyuria, and how does it relate to her diagnosis?
• What electrolyte imbalances do you suspect are found on Lisa’s CMP (use terms, not specific values)?
  • Hypothesize and explain the cause for the imbalances
  • Name 2 symptoms Lisa might experience as a result of these imbalances (that have not already been described in the prompt)
• What alterations do you think Lisa may have in her acid-base balance?  
  • Hypothesize and explain the cause for the imbalances
  • Name 2 symptoms Lisa might experience as a result of these imbalances (that have not already been described in the prompt)
• What mechanisms could be driving Lisa’s low blood pressure? Please explain the altered physiology behind the mechanism.

Answer 1

1.Pyuria is defined as the presence of 10 or more white blood cells(WBCs) per cubic millimeter in a urine specimen, 3 or mone white cells per high power field of unspun urine, a positive result on gram staining of an unspun urine specimen or a urinary dipstick test that is positive for leuocyte esterase

She is diagnosed with pyelonephritis , infalmmation of renal parenchyma caused by bacteria, fungi, protozoa or virus. urosepsepsis is a sytemic infection arising from a urologic source. It can lead to septc shock and death unless promptly eradicated. Septic shock is the outcome of unresolved bactremia involving a gram negative organism

2.

Laboratory study	Findings	Significance of finding
Serum electrolytes S.Sodium S.Potassium	Hypernatremia Hyponatremia Hyperkalemia Hypokalemia	hypernatremia found in early stages of shock because of increased secretion of aldosterone Hyponatremia may occur iatrogenically when excess hypotonic fluid is administered after fluid loss Hyperkalemia results when cellular death liberated intracellular death Hypokalemia found in early shock because of increased secretion of aldosterone, causing renal excretion of potassium
Arterial Blood Gases	Respiratory alkalosis Metabolic acidosis	found in early shock secondary to hyperventilation Metabolic acidosis occurs later in shock when lactate accumulates in blood from anaerobic metabolism
Base deficit	> -6	indicates acid production secondary to hypoxia
Blood cultures	Growth of organisms	may grow organisms in patients who are in shock
Liver enzymes	ALT, AST,GGT	elevations indicate liver cell destruction in progressive stage of shock

3.

clinical manifestations of septic shock

System affected	signs and symptoms
cardiovascular system	tachycardia decreased BP decreased capillary refil chest pain may or may not present
pulmonary system	Hyperventillation crackles ,respiratory acidosis leads to shortness of breath cyanosis Hypoxemia respiratory failure ,ARDS
Renal system	Increased sodium and water retention decreased renal blood flow decreased urine output
Skin	pallor cool clammy
Neurologic sytem	Decreased cerebral perfusion alteration in mental status(confusion,agitation) Coma(late)
Gastrointestinal sytstem	decreased bowel sounds nausea vomiting GI bleeding paralytic illeus

4. septic shock is the presence of sepsis with hypotension despite adequate fluid resuscitation along with inadequate tissue perfusion resulting in tissue hypoxia

Septic shock has 3 major pathophysiologic effects:

• Vasodilation
• maldistribution of blood flow
• myocardial depression

patients may be euvolemic, but because of acute vasodilation, relative hypovolemia and hypotenion occur. In addition,blood flow in the microcirculation is decreased, causing poor oxygen delivery and tissue hypoxia

The combination of Tumor necrosis factor and interleukin-1 is thought to have a role in sepsis -induced myocardial dysfunction. The ejection factor is decreased for the first few days after the initial insult. Because of decreased ejection fraction ventricles dilate to maintain the stroke volume. The ejection fraction typically improves and ventricular dilation resolves over 7-10 days. Persistence of high cardiac output and a low SVR beyond 24 hrs is an omnious finding and is often associated with devlopment of hypotension