Question

– ACUTE CARE CASE STUDY

Patient and Setting: CM is a 45-year-old man, on an inpatient surgical unit

Chief Complaint: Sudden onset of nausea/vomiting, some difficulty breathing, change in status

History of Present Illness: CM is in hospital, day 2 post-ORIF fractured femur with significant haemorrhage and other soft tissue injuries, sustained in an MVA.  CM reports that his feet are swelling, (+) fatigue, (+) nausea and vomiting, and (+) SOB. He has also noticed a decrease in urine output , although he reports he has not been eating or drinking much.

Medical History: Hypertension (×5 yrs), MVA

Surgical History: N/A (other than current hospitalization)

Family History: Mother: DM; Father: died at age 50 due to MI

Social History: Ethanol intake: Nil; tobacco: once/month

Medications:

Lisinopril 40 mg PO BID for 5 years

ASA 81 mg po daily

Rosuvastatin 20mg po daily

Amlodipine 10 mg PO QD for 2 years

Ibuprofen 800 mg PO TID for back pain

Centrum One 1 tab PO QD

Allergies: Morphine (tongue swelling, itching, rash, SOB)

Physical Examination:

GEN: Well-developed, nourished man

VS: BP 190/100, HR 83, RR 26, T 37.3°C, Wt 80 kg, Ht 182 cm

HEENT: WNL

CHEST: Small crackles, rales, and wheezing

ABD: WNL

EXT: Bilateral LE swollen with fluid, 3+ pitting edema

NEURO: A & O ×2 (place, time)

Results of Pertinent Laboratory Tests, Serum Drug Concentrations, and

Diagnostic Tests:

Na 132 K 5.9  

Hgb 88 Hct 0.34   Creatinine 189 BUN 23  

Blood Gas: pH 7.3; pCO2 40; HCO3 18; pO2 97

Urine Output: 300 mL/24 hr

Question:

1. Classify CM’s acute renal failure as prerenal, intrarenal, or postrenal and justify your answer.

Note: pleas answer the question with great detail from the case study and with rational because I posted this question couple days ago and I got an incomplete answer someone just copy paste from google. I don't need that kind of answer. I said that cuz I don't want to get another incomplete answer. Thank you.

Thanks for the comment all the lab results are correct.

Answer 1

Acute kidney injury

Acute kidney injury is characterized by abrupt deterioration in kidney function, manifested by an increase in serum creatinine level with or without reduced urine output. The spectrum of injury ranges from mild to advanced, sometimes requiring renal replacement therapy. The diagnostic evaluation can be used to classify acute kidney injury as prerenal, intrinsic renal, or postrenal. The initial workup includes a patient history to identify the use of nephrotoxic medications or systemic illnesses that might cause poor renal perfusion or directly impair renal function. Physical examination should assess intravascular volume status and identify skin rashes indicative of systemic illness. The initial laboratory evaluation should include measurement of serum creatinine level, complete blood count, urinalysis, and fractional excretion of sodium. Ultrasonography of the kidneys should be performed in most patients, particularly in older men, to rule out obstruction. Management of acute kidney injury involves fluid resuscitation, avoidance of nephrotoxic medications and contrast media exposure, and correction of electrolyte imbalances. Renal replacement therapy (dialysis) is indicated for refractory hyperkalemia; volume overload; intractable acidosis; uremic encephalopathy, pericarditis, or pleuritis; and removal of certain toxins. Recognition of risk factors (e.g., older age, sepsis, hypovolemia/shock, cardiac surgery, infusion of contrast agents, diabetes mellitus, preexisting chronic kidney disease, cardiac failure, liver failure) is important. Team-based approaches for prevention, early diagnosis, and aggressive management are critical for improving outcomes.

Etiology

The causes of acute kidney injury can be divided into three categories :

• prerenal (caused by decreased renal perfusion, often because of volume depletion),
• intrinsic renal (caused by a process within the kidneys),
• postrenal (caused by inadequate drainage of urine distal to the kidneys).

In patients who already have underlying chronic kidney disease, any of these factors, but especially volume depletion, may cause acute kidney injury in addition to the chronic impairment of renal function.

Here in this case

CM is a 45-year-old man, on an inpatient surgical unit with chief complaint Sudden onset of nausea/vomiting, some difficulty breathing,he is in hospital, day 2 post-ORIF fractured femur with significant haemorrhage and other soft tissue injuries, sustained in an MVA.he is having a urine output of 300/hr suggest kidney disease. His feet are swelling and having 5 year history of hypertension.currently he is taking NSAID( ibuprofen) and  ACE inhibitor(lisinopril). for back pain.from these observation he is diagnosed with a prerenal type of acute kidney disease.

pre renal causes of acute kidney disease

• Intrarenal vasoconstriction (hemodynamically mediated)
• Medications: nonsteroidal anti-inflammatory drugs,* angiotensin-converting enzyme inhibitors,* angiotensin receptor blockers,* cyclosporine (Sandimmune), tacrolimus (Prograf)
• Cardiorenal syndrome*
• Hepatorenal syndrome
• Abdominal compartment syndrome
• Hypercalcemia
• Systemic vasodilation (e.g., sepsis,* neurogenic shock)
• Volume depletion
• Renal loss from diuretic overuse,* osmotic diuresis (e.g., diabetic ketoacidosis*)
• Extrarenal loss from vomiting, diarrhea,* burns, sweating, blood loss

Approximately 70 percent of community-acquired cases of acute kidney injury are attributed to prerenal causes.10 In these cases, underlying kidney function may be normal, but decreased renal perfusion associated with intravascular volume depletion (e.g., from vomiting or diarrhea) or decreased arterial pressure (e.g., from heart failure or sepsis) results in a reduced glomerular filtration rate. Autoregulatory mechanisms often can compensate for some degree of reduced renal perfusion in an attempt to maintain the glomerular filtration rate. In patients with preexisting chronic kidney disease, however, these mechanisms are impaired, and the susceptibility to develop acute-on-chronic renal failure is higher.

Several medications can cause prerenal acute kidney injury. Notably, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers can impair renal perfusion by causing dilation of the efferent arteriole and reduce intraglomerular pressure. Nonsteroidal anti-inflammatory drugs also can decrease the glomerular filtration rate by changing the balance of vasodilatory/vasoconstrictive agents in the renal microcirculation. These drugs and others limit the normal homeostatic responses to volume depletion and can be associated with a decline in renal function. In patients with prerenal acute kidney injury, kidney function typically returns to baseline after adequate volume status is established, the underlying cause is treated, or the offending drug is discontinued.