AKI :

Rapid decrease in the kidney’s ability to eliminate waste products such as urea and creatinine. Other manifestations include decreased urine output, metabolic acidosis and hyperkalemia.

It can be defined and classified using changes in s. creatinine levels and urine output using the RIFLE criteria. This divides AKI into categories of RISK, INJURY, FAILURE, LOSS and END STAGE KIDNEY DISEASE.

CLINICAL CLASSIFICATION

Prerenal Renal (Parenchymal or Intrinsic) Postrenal

PRERENAL RENAL FAILURE:

Initial stage. It is functional in nature. Kidneys malfunction because of systemic factors that decreases GFR (decreased cardiac output, hypotension, sepsis etc.)

If the systemic cause is removed , renal function improves and relatively rapidly returns to normal levels.

If intervention is delayed or unsuccessful, renal injury becomes established (structural) and several days or weeks are required for recovery.

PARENCHYMAL RENAL FAILURE:

Principal source of damage is within the kidneys and structural changes can be seen in microscopy.
Causes of parenchymal AKI : GLOMURELONEPHRITIS

• VASCULITIS
• INTERSTITIAL NEPHRITIS
• MALIGNANT HYPERTENSION
• PYELONEPHRITIS
• BILATERAL CORTICAL NECROSIS
• AMYLOIDOSIS
• MALIGNANCY
• NEPHROTOXINS
• CHOLESTROL EMBOLISM
• Removal of nephrotoxins rapidly improves AKI.

Most common type of intrinsic AKI falls under ACUTE TUBULAR NECROSIS. It is assumed that tubular necrosis results from continuous hypoperfusion.

HEPATORENAL SYNDROME:

This form of AKI develops in severe liver dysfunction in the absence of other known causes of ARF. It presents as progressive oliguria with a very low sodium concentration (

Newer concensus defines HRS as any development of AKI in the setting of advanced liver disease that is not due to intrinsic causes.

RHABDOMYOLYSIS:

Pathogenesis includes prerenal, renal, postrenal factors. It is seen following major trauma , drug overdose, vascular embolism and in response to various agents that can induce major muscle injury.

Treatment include prompt and aggressive fluid resuscitation, elimination of causative agent, correction of compartment syndromes, alkalinisation of urine (pH>6.5) and the maintenance of polyuria (>300 ml/h).

POSTRENAL RENAL FAILURE:

Obstruction to urine outflow is the most common cause of functional renal impairment in the community but uncommon in the ICU. However sudden and unexpected anuria in ICU patients should always suggest obstruction of urinary catheter.

DRUGS CAUSING AKI IN ICU

• RADIOCONTRAST AGENTS
• AMINOGLYCOSIDES
• AMPHOTERICIN
• NSAIDS
• BETA LACTUM ANTIBIOTICS
• SULFONAMIDES
• ACYCLOVIR
• METHOTROXATE
• CISPLATIN
• CYCLOSPORIN A
• TACROLIMUS
• SIROLIMUS
• STARCH SOLUTIONS

RESULTS AND DISCUSSIONS:

AKI is a common occurrence in ICU. In this study of 200 patients being admitted to Medical ICU it was found that 94% of them were admitted with AKI. Around 6% developed AKI in ICU causes ranging from drugs to hypovolemia.
Of these 200 patients 78% were males and 22% females.

Age wise distribution showed an incidence of 46% in the elderly group of age more than 65, 35% in age group 45-60, 16% in 30-45 and 3% in 15-30 years of age. In the younger population GN was found to be the most common cause.

79% of these patients had a known CKD background whereas 21% were found to have AKI on non CKD.
Sepsis was found to be the most common cause having an incidence of around 56%. Heart failure was found to have an incidence of 16% followed by ACS with 13% occurrence. Other causes include HRS and GN with 4%, hypovolemia 3%, drugs with 2% and DKA and Snake bite with 1% each.

Hemodialysis was done for 33% of these patients and 67% were managed without  any RRT.

61% of these patients were discharged from ICU and 17% opted for self-discharge (LAMA). The mortality in these 200 patients was found to be around 26%.

Of the total number of deaths 45% underwent hemodialysis and 55% were managed without RRT.

The percentage of patients developing AKI after admission was found to be 6%. The mortality rate in this group was 33% of whom all the patients had dialysis.

CONCLUSIONS:

AKI has been found in early 20th century medical literatures being described as War Nephritis. Despite of such early recognition research has been not extensive due to contrasting and contradictory definitions.

This changed with the introduction of the RIFLE criteria for AKI in 2004 by the Acute Dialysis Quality Initiative (ADQI). This defined AKI with changes in the S. CREATININE levels and urine output of the patient. Now RIFLE criteria is widely used in ICUs to assess AKI. The incidence of AKI has been on a rise probably due to better detection and recognition. Still it is one of the most under reported  entities in the ICU.  Mortality in ICU was about 26% and patients developing AKI after admission had a greater mortality rate although dialysis was done for these patients. The study was limited by the total number of patients who developed AKI post admission. Further study is required to identify those patients developing AKI in ICU, mortality in these patients and modifiable risk factors.

REFERENCES:

1. Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Critical Care. 2007;11, article R31
2. Ostermann M, Chang RWS. Acute kidney injury in the intensive care unit according to RIFLE. Critical Care Medicine. 2007;35(8):1837–1843
3. Hoste EAJ, Clermont G, Kersten A, et al. RIFLE criteria for acute kidney injury are associated with hospital mortality in critically ill patients: a cohort analysis. Critical Care. 2006;10

Author:

DR. Manash Ranjan Chaudhury
Fellow, Critical care Medicine
Narayana Superspeciality Hospital
Guwahati, Assam

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Introduction: The reported incidence of acute kidney injury after rhabdomyolysis is as high as 65%¹ which occurs as a result of multiple mechanisms including tubular obstruction, direct and ischemic tubular injury, or intrarenal vasoconstriction. In this report, we present a case of acute kidney injury induced by rhabdomyolysis in a young male post-trauma.

Presentation: A 37 yr old male patient presented to the emergency department with a history of trauma and physical assault 4 days back, multiple wounds all over the body and reduced urine output for 1 day. On examination he was found to have generalised swelling all over the body, multiple bruises and abrasions along with fracture of right 4^th metatarsal bone. Laboratory studies revealed CPK: 17345 IU/L; BUN: 79mg/dl; Serum creatinine: 11.35mg/dl; Serum potassium: 4.1meq/L; Urine Ph: 5. Adequate hydration was started with balanced salt solution and 0.9% NS also haemodialysis was done with which the patient’s renal functions improved gradually.

Conclusion: Rhabdomyolysis induced AKI in a patient with no co morbidities resolves gradually with adequate hydration and urine output monitoring.

Introduction:

Rhabdomyolysis is a clinical condition in which skeletal muscles break down rapidly releasing toxic substance like creatine kinase and myoglobin into the blood stream which in turn leads to kidney injury. This can happen because of sustained trauma, sepsis, heat stroke or even drugs.

Pathophysiology:

Rhabdomyolysis involves direct sarcolemic injury leading to depletion of ATP within the myocyte which impairs the function of ATPase pump. This causes an increased sarcoplasmic calcium levels leading to a state of persistent contraction of the myofibril. This sustained contraction leads to further energy depletion.

After myocyte injury, intracellular contents are released into the circulation.^{2, 3}   Hyperkalaemia, hyperuricaemia, and hyperphosphataemia can develop rapidly. High levels of phosphate released in blood; bind to calcium, and calcium–phosphate deposition occur in soft tissue, resulting into hypocalcaemia. Ischemic muscle is also forced to utilise anaerobic metabolism leading to metabolic acidosis.

During the recovery phase of rhabdomyolysis, significant number of patients develop hypercalcaemia, due to the release of vitamin D stores from injured muscle, providing substrate for the production of excess 1,25-dihydroxyvitamin D^4.  Hypercalcaemia may be further exacerbated if excess calcium is administered during the acute hypocalcaemic phase.

Myoglobin a dark red haem-containing protein stores and transports oxygen in muscle. Only small levels of it are normally present in plasma. It has a small molecular weight and is easily filtered. When the renal threshold for free myoglobin is exceeded it appears in urine.⁵ This then interacts with the Tamm–Horsfall proteins to form brown granular casts resulting in tubular obstruction. The process is favoured when the urine is acidic and may have no nephrotoxic effect when the urine is alkaline.

Myoglobin also causes deficit of nitric oxide leading to renal vasoconstriction which further compounds to kidney injury. Renal blood flow is further compromised by hypovolaemia, activation of the renin–angiotensin system, and additional vascular mediators. ²

Clinical features:

Severity of symptoms depends upon the degree of muscle damage and extent of kidney injury. Rhabdomyolysis may be asymptomatic or associated with muscle pain, nausea, sepsis, dyselectrolytemia, arrythmia, acute renal failure and even coma. A high degree of suspicion is needed from prompt management and avoidance of complications arising. Severe pain may at times limit limb movement and additionally in compartment syndrome or crush injury the muscles may get tense and swollen, leading to a sensoryneural loss. In diffuse muscle injury such as which occurs with drugs, there may be a generalised malaise with diffuse myalgia. Rarely, patients may volunteer that their urine has changed to a red or brown colour.

Lab findings:

Rhabdomyolysis is typically diagnosed when the CK is more than 5000 units/litre or five times its normal upper limit. Myoglobin levels peak before increases in CK, however, myoglobin is metabolised rapidly at sites outside of the kidney hence CK a more reliable marker of rhabdomyolysis. The absence of myoglobinuria does not rule out the possibility of rhabdomyolysis. In a study of 475 patients with rhabdomyolysis diagnosed by CK levels, myoglobinuria was only detected in 19%⁶  A Metabolic Acidosis with high anion gap is usually observed. Arterial blood gases also reveal trend of serum lactate and pH and serves as a guide for fluid replacement. Regular observations including hourly urine output are required to detect any deterioration promptly.

Case Report:

A 37 year old male, with no comorbidities, presented to the emergency department with complains of reduced urine output for 1 day, there was an associated history of physical assault 4 days back in which he suffered multiple contusions and abrasions all over his body along with a  fracture of right 4^th metatarsal bone, for which orthopaedic consult was taken. He was admitted to the critical care department and his initial laboratory studies revealed CPK: 17345 IU/L, BUN: 79mg/dl, Serum creatinine: 11.35mg/dl, Serum Potassium: 4.1meq/L, Urine Ph: 5, Serum Calcium: 7.2mg/dl, Serum Phosphorus: 7.6mg/dl.

Foley’s catheterization was done and central venous access was taken. Keeping myogologinuria induced rhabdomyolysis in mind he was thereafter managed primarily with fluid resuscitation with a target urine output of 3 ml/kg/hr or 300 ml/hr. 0.9% Normal saline, balanced salt solution was used while monitoring potassium and arterial blood gases to look for hyperchloraemic acidosis.

Continuous infusion of soda bicarbonate was initiated to alkalinise the urine to reduce the precipitation of Tamm–Horsfall protein complexes. A urinary pH of 7 was achieved on day 2 of the treatment. We also initiated infusion of Inj furosemide at 5-10 mg/hr to maintain an adequate urine output.

The patient was evaluated by a nephrologist and haemodialysis was initiated on day 2 and day 4 of admission, soda bicarbonate and furosemide was gradually tapered off with close monitoring of urine output. Fluid resuscitation continued, as guided by IVC dimensions. The patients renal functions improved gradually and he was later discharged in a stable condition with adequate urine output, with a serum creatinine of 2.59mg/dl and CPK: 150 IU/L.

Discussion:

We have reported a case of Acute kidney injury due to trauma induced rhabdomyolysis, patient here landed up into AKI due to dehydration and inadequate fluid resuscitation, which eventually resolved with intravenous hydration therapy. Another contributing factor of adequate recovery was young age of the patient with no history of any comorbidities or drug intake which could have been be a secondary cause of renal dysfunction.

Evidence for the use of sodium bicarbonate as a therapy to prevent AKI in rhabdomyolysis is lacking. A recent systematic review found no level 1–3 evidence to support its use.

Mannitol also has theoretical benefits by flushing nephrotoxic agents through the tubules, it extracts fluid that has accumulated in injured muscle, and acts as a free radical scavenger. Again there was no level 1–3 evidence to support the use of mannitol in the prevention of AKI^7.

Considering the benefit achieved by alkalising the urine and forced diuresis soda bi carbonate and furosemide infusion was used in this patient. Further studies may be needed to clarify this effect.

Hence, we conclude stating the primary treatment of Acute kidney injury induced by rhabdomyolysis being vigorous fluid resuscitation with intensive urine output monitoring.

References:

1. Meijer AR, Fikkers BG, Keijzer MH, Engelen BG, Drenth JP. Serum creatine kinase as predictor of clinical course in rhabdomyolysis: a 5-year intensive care survey. Intensive Care Med 2003; 29: 1121–5
2. Holt SG, Moore KP. Pathogenesis and treatment of renal dysfunction and rhabdomyolysis. Intensive Care Med 2001; 27: 803–11.
3. Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med 2009; 361: 62–72
4. Akmal M, Bishop J, Telfer N, Norman AW, Massry SG. Hypocalcaemia and hypercalcaemia in patients with rhabdomyolysis with and without acute renal failure. J Clin Endocrinol Metab 1986; 63: 137–42
5. David WS. Myoglobinuria. Neurol Clin 2000; 18: 215–43
6. Melli G, Chaudhry V, Cornblath DR. Rhabdomyolysis: an evaluation of 475 hospitalized patients. Medicine (Baltimore) 2005; 84: 377–85
7. Scharman EJ, Troutman WG. Prevention of kidney injury following rhabdomyolysis: a systematic review. Ann Pharmacother 2013; 47: 90–105)

Abbreviations :

AKI : Acute Kidney Injury

CPK : Creatinine Phospho Kinase

CK : Creatinine Kinase

BUN : Blood Urea Nitrogen

ATP : Adenosine Tri Phosphate

NS : Normal Saline

IVC : Inferior Vena Cava

Author:

Dr. Sujan Dey, Consultant Critical Care, Artemis Hospitals, Gurugram.
Dr Reshma Tewari,Director Critical Care,Artemis Hospitals,Gurugram
Dr. Urvashi Modi, Registrar Critical Care, Artemis Hospitals, Gurugram.
Dr Muneer Jan,Assoc.Consultant Critical Care,Artemis Hospitals, Gurugram
Dr. Abhishek Goyal, Registrar Medicine, Artemis Hospitals, Gurugram.

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