Differential Diagnosis I: Septic Shock
Description:
“Septic Shock is the endpoint of a continuum of progressive dysfunction. The disease process begins with infection entering the bloodstream and causing bacteremia. Septic Shock is commonly associated with both systemic inflammatory response syndrome (SIRS) and sepsis with multiorgan dysfunction” (McCance & Huether, 2019, p.1550).
Common clinical manifestations of septic Shock include altered mental status, hypotension despite vasopressors, tachycardia, tachypnea, elevated white blood cells, fever, elevated lactate and increased creatinine.
Rationale:
The patient’s recent history of fever, purulent drainage of foot wound, general malaise, and elevated sepsis markers aid in the decision to include septic shock amongst our differential diagnoses. Additionally, patient presented with elevated creatinine, lactate, C-reactive protein, and lethargy upon admission to MICU. The patient’s blood pressure was unresponsive to IVF bolus, indicating a need for vasopressor therapy. Furthermore, the X-ray and MRI of the foot demonstrated soft tissue inflammation and concern for osteomyelitis, indicating an infectious cause.
Figure 1: Sepsis Definition and Criteria McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biological basis for disease in adults and children (8th ed.). St. Louise, MO: Mosby.
Differential Diagnosis II: Hyperosmolar Hyperglycemia Nonketotic Syndrome (HHKS)
Description:
HHKS is a complication of type two diabetes mellitus. It is often caused by uncontrolled blood sugars and can be precipitated by cardiovascular disease, renal disease, or infection or illness (McCance & Huether, 2019). HHKS results from insulin deficiency and increased levels of hormones that work against insulin that stimulate the production of glucose, breakdown of glycogen to glucose, decreased glucose uptake by peripheral tissues such as muscle and is characterized by a lack of ketosis.
Predisposing factors include those of young age, undiagnosed person’s with diabetes mellitus type II, and geriatric individuals with comorbidities such as infection, cardiovascular disease, and kidney disease (McCance & Huether, 2019). Clinical manifestations of HHKS include glycosuria, polyuria, dehydration (increased serum osmolarity), lethargy, hypotension, tachycardia, weakness, and elevated BUN and creatinine. Diagnostic factors include blood sugar >600mg/dL, a near normal serum bicarbonate level and pH, serum osmolarity >320 mOsm/L, and either absent or low levels of ketones in the urine and blood.
Rationale:
The patient’s history of uncontrolled type two diabetes mellitus, obesity, hypertension, elevated blood sugar of 424mg/dL, and the concern for infection of the patient’s foot ulcer puts the patient at risk for HHKS. Common clinical manifestations of HHKS that are exhibited by our patient include elevated blood sugars, tachycardia, hypotension, dehydration, and drowsiness.
The patient, however, is not experiencing blood sugars >600mg/dL and his pH is on the acidic side. Therefore, this may indicate that another disease process.
Figure 2: Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHKS) Source: McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biological basis for disease in adults and children (8th ed.). St. Louise, MO: Mosby.
Differential Diagnosis III: Acute Pancreatitis
Description:
Acute pancreatitis is caused by bile or pancreatic duct obstruction causing pancreatic secretions to back up into the pancreas (McCance & Huether, 2019). These secretions stimulate the activation and release of pancreatic enzymes that promote autodigestion of pancreatic cells leading to inflammation and edema that can cause ischemia and necrosis. Inflammation of the acinar cells of the pancreas leading to a systemic response.
Risk factors that place patients at risk for developing acute pancreatitis include age 50-60 years old, alcoholism, cholelithiasis, peptic ulcers, abdominal trauma, hyperlipidemia, and smoking. The most common clinical manifestation of acute pancreatitis is epigastric/mid-abdominal pain. Systemic signs and symptoms include fever, leukocytosis, nausea, vomiting, tachypnea, tachycardia, and hyperglycemia. Furthermore, other signs are jaundice, abdominal distension, and bowel hypomotility. Lab results that indicate pancreatitis are elevated amylase, lipase, and C-reactive protein (CRP).
Rationale:
Mr. S.S. is at risk for developing pancreatitis due to his age, history of alcoholism, history of hyperlipidemia, and smoking status.The patient is presenting signs such as abdominal pain, fever, tachycardia, tachypnea, hyperglycemia, hypovolemia as well as an elevated CRP, which may indicate that the patient is experiencing acute pancreatitis.
Patient S.S., however, did not show elevated lipase or amylase levels, which are typically diagnostic for acute pancreatitis. Thus, our patient is likely experiencing another diagnosis.
Figure 3: Pathophysiology of Acute Pancreatitis Source: McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biological basis for disease in adults and children (8th ed.). St. Louise, MO: Mosby.
Differential Diagnosis IV: Hypovolemic Shock
Description:
Hypovolemic shock results from a major loss of whole blood or plasma (direct) or interstitial fluid (indirect) (McCance & Huether, 2019). Whole blood or plasma loss directly decreases intravascular content causing hypovolemia and poor perfusion while loss of interstitial fluid causes indirect (“relative”) hypovolemia by promoting diffusion of plasma from the intravascular space to the to the extracellular space.
A patient experiencing hypovolemic shock will, initially, compensate for this intravascular loss by increasing their heart rate and systemic vascular resistance (SVR or vasoconstriction) (McCance & Huether, 2019). This occurs as the adrenal glands release catecholamines in efforts to improve cardiac output (CO) and tissue perfusion pressure to ensure the organs are receiving adequate nutrients. The liver and spleen attempt to increase blood volume by producing more red blood cells (RBCs), and the kidneys induce the renin-angiotension adolesterone system to increase water retention as a mechanism to increase intravascular content. As hypovolemic shock progresses, these compensatory mechanisms fail, resulting in decreased tissue perfusion and failed cellular metabolism.
Clinical manifestations associated with hypovolemic shock include poor skin turgor, diffuse vasoconstriction, pallor, cool extremities, decreased preload, thirst, oliguria, and tachycardia (McCance & Huether, 2019).
Rationale:
Mr. S.S. may be experiencing an indirect loss of fluid by means of his draining foot wound. He presents with tachycardia, low urine output, and poor skin turgor. The patient also has low urine output and poor skin turgor. The patient could be beginning to show signs of failing compensatory mechanisms with their vitals. Ruling out hypovolemic shock will help with the correct treatment of the patient.
What doesn’t fit with this diagnosis is that the patient has an infection, elevated WBC and lactate, and abdominal pain. Additionally, the patient complains of feeling sweaty and appears flushed rather than presenting with pallor. The likelihood that the patient is experiencing hypovolemic shock from a draining foot wound is low; however, it is important to rule out.
Figure 4: Hypovolemic Shock Source: McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biological basis for disease in adults and children (8th ed.). St. Louise, MO: Mosby.