Volume 3 - Issue 11-2

Recognize Rhabdomyolysis early to prevent Acute Kidney Injury and Acute Renal Failure

Department of Emergency Medicine and Critical Care, Kauvery Specialty Hospital, Cantonment, Trichy, India

Department of Nephrology, Kauvery Specialty Hospital, Cantonment, Trichy, India

Department of Neurosurgery and Neurology, Kauvery Specialty Hospital, Cantonment, Trichy, India

Abstract

Acute Kidney Injury (AKI) is a complication of rhabdomyolysis. In this article, we discuss the case of a 31-year-aged male who was found unresponsive and brought to ER in an unconscious state by an unknown person, who developed acute kidney injury and needed dialysis for long-duration. This case review emphasizes the importance of recognizing rhabdomyolysis in an unresponsive patient with severe metabolic acidosis, its aggressive management, and a thorough understanding of the precipitating causes of rhabdomyolysis in order to prevent acute renal injury which in turn may even lead to a potentially lethal complication-ESRD (end stage renal disease)

Background

Acute Kidney Injury is a complication of rhabdomyolysis, which in turn results from muscle injury. Signs and symptoms of Rhabdomyolysis are muscle pain, red, brown, or high colored urine, and elevated serum muscle enzymes (creatine kinase, LDH etc.). Other signs include abnormalities in fluid and electrolyte abnormalities, many of which may precede kidney failure. Other complications of rhabdomyolysis include cardiac dysrhythmias, liver injury, and compartment syndrome, and disseminated intravascular coagulation may develop over the course. Acute renal failure is a complication experienced by 5 to 25% of patients undergoing rhabdomyolysis. One episode of seizure, for e.g. generalized tonic-clonic seizure, can rarely cause rhabdomyolysis. Most of the cases of rhabdomyolysis that are reported in the literature are following status epilepticus/ prolonged seizure, accompanied by dehydration. Rhabdomyolysis can be asymptomatic; hence high clinical suspicion is warranted to prevent later complications including acute kidney injury or even End Stage Renal Disease. We report here a case of acute renal failure due to rhabdomyolysis that occurred after suspected seizures.

Case Presentation

A 31-years- aged male was brought to ER around 10 am, with alleged h/o being found unresponsive in his room by his house owner. He was last seen normal at about 8 pm, the previous day. He had h/o RTA 4 years ago s/p Craniotomy and was on anti-epileptic medications.

On arrival, the patient was cyanosed, with cold peripheries. BP was not recordable, and so was SpO2. No visible traumatic injury and no ligature mark present. PR, 88/min; GCS E1 V1 M1, 3/15; and pupils B/L, 2 mm; reacting equally.

His sugar levels were normal.

He was intubated and put on a mechanical ventilator. Fluid resuscitation was done aggressively, and ionotropes infusion began for hypotension. He was started on empirical antibiotics. CT Brain showed post-operative changes in the frontal region and adjacent gliosis, post-operative changes in maxillary, and ethmoid sinuses with mini plate insitu.

Neurologist advised the patient to be placed on anti-epileptic medication. His initial labs were negative for both infective etiologies and toxicology.

In the initial few hours, urine output was adequate and urine color was normal. Rhabdomyolysis was suspected because of persistent metabolic acidosis, the patient's history of the neurosurgical procedure, possible seizure episodes overnight, and possible dehydration.

Relevant tests were ordered. Marked elevation in CPK levels was noted as 7240 U/L. Urine myoglobin was also positive. His Urea and Creatinine, upon presentation to ER,were mildly elevated.

Patient was shifted to ICU for further care and started on forced alkaline diuresis. Sensorium improved, GCS - 10T/15.

On day 2 of hospitalization, his urine output was adequate, he had an elevated total count and CT chest suggestive of aspiration pneumonitis. Tracheal, blood, and urine cultures were negative. He was extubated on day 3 of admission.

His urea creatinine increased with oliguria and worsening acidosis. He needed intermittent NIV support due to pulmonary edema which developed due to AKI. Hemodialysis was initiated on day 5 of hospitalization. CPK levels were periodically checked and were found to be on a decreasing trend. Nephrologists, Urologists, and cardiologists were involved in the course of treatment, Orthopedician had ruled out compartment syndrome and bony injury. Patient was weaned off of NIV support, 12 cycles of hemodialysis were done in total during his hospital stay. Patient's general condition improved and became hemodynamically stable.

He was discharged on the 26th day of admission, after explaining the need to continue hemodialysis in view of the persistently elevated urea/creatinine levels. Renal biopsy was suggested by nephrologist, to be done later.

Table 1. On examination

 Day of admission

1

3

7

9

13

15

17

19

21

24

Urea Serum (normal value:10-50 mg/dL)

51.5

87.4

127.2

184.1

180.0

172.9

168.5

170.8

131.8

157.0

Creatinine Serum (normal 0.5-1.4 mg/dl )

2.34

6.29

8.18

8.99

7.48

7.93

9.04

8.69

7.33

9.01

Urine output (mls/h)

100

60-90

15-30

15-30

10

25

25-30

40-50

50-60

50-60

RBCs in Urine (normal 0)

Nil

65-70

80-90

30-35

6-8

 

 

 

 

 

CPK (Normal: 0-195 U/L)

7240

157350

362000

310250

6400

3100

1000

 

400

 

SGOT (normal 0-35)

1459

 

 

442

 

 

 

 

 

 

SGPT (normal 0-45)

309

 

 

321

 

 

 

 

 

 

Table 2. Acid Base Gases (ABG).

Day of admission

upon presentation to ER

5 h after the presentation

8 h after the presentation

1

2

3

4

5

6

10

12

13

22

pH-Blood

7.37

7.36

7.24

7.32

7.55

7.52

7.57

7.49

7.44

7.46

7.51

7.49

7.40

PCO2  (mmHg)

27

23

43

41

42

51

44

39

41

27

30

25

32

HCO3 std (mmol/L)

18.8 

17.1

16.8

20.0

35.0

37.7

37.7

29.5

26.4

21.9

25.9

22.5

21.3

CT brain image of patient showing post-operative changes in frontal region and adjacent gliosis

Fig. 1. CT brain image of patient showing post-operative changes in frontal region and adjacent gliosis.

Discussion

Rhabdomyolysis is a potentially fatal condition that may arise from traumatic causes (multiple trauma, crush injuries, surgery, immobilization etc.) and non-traumatic causes (extreme exertion, heat stroke, snake bite, decreased blood perfusion to the muscle tissue, infections, muscle diseases including hereditary enzyme deficiencies imbalance of electrolytes, hyperkinetic states, seizures, drugs, toxins, snake bite, Bee sting, neuropathies, malignant neuroleptic syndrome etc.) [1,2,9]. The pathology of rhabdomyolysis is muscle cell death, which could be due to any of the above reasons.

The final pathway of muscle tissue injury is in two ways: 1. Decrease in ATP (adenosine triphosphate, cellular source of energy) leading to intracellular, cytoplasmic, free ionized calcium as well as mitochondrial calcium increase, thereby leading to myocyte injury, 2. Direct injury and rupture of the plasma membrane.

Damage to muscle tissue causes the release of intracellular muscle contents, including creatine kinase (CK) and other muscle enzymes (aldolase, aldolase, lactate dehydrogenase (LDH), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) etc.), myoglobin, and various electrolytes, which can be measured in the lab and indicate muscle injury.

In this case, rhabdomyolysis could be due to seizure episodes. Seizure activity leads to excessive ATP utilization and ATP production cannot keep up with the demand hence ATP gets depleted. Due to ATP depletion and sodium-potassium ATPase pump failure, the integrity of sarcolemma (muscle cell membrane) will be lost and will ultimately lead to rhabdomyolysis [3]. Rhabdomyolysis is a frequent occurrence after muscle injuries but it is usually asymptomatic in minor injuries. However, in more serious cases, severe electrolyte disorders and acute renal failure may occur, leading to life-threatening situations.

Signs and symptoms of rhabdomyolysis can be theoretically described as a triad of myalgia, fatigue, cola colored urine. These clinical manifestations are non-specific and may not be always present. So there needs to be a high level of suspicion and relevant lab tests should be ordered which are essential for early diagnosis. Rhabdomyolysis lab findings include elevated CK and other serum muscle enzymes. The sensitive test of rhabdomyolysis and myocyte injury is CK levels [5], whose normal levels in blood are 0 to 195 U/l.

12 h of onset of muscle injury

CK starts to rise

1-3 days

CK peaks

3-5 days after cessation of muscle injury

Ck declines

Half-life of CK is about 36 h and declines at a relatively constant rate of about 40 % of previous days value after cessation of muscle injury.

CPK elevations are frequently classified as mild, moderate, or severe.

Mild

less than 10 times the upper limit of normal (or 2,000 IU/L)

Moderate

10 to 50 times the upper limit of normal (or 2,000 to 10,000 IU/L)

Severe

greater than 50 times the upper limit of normal (or greater than 10,000 IU/L)

The risk of renal failure increases above 5,000 to 6,000 IU/L [6]. In our patient, CK level at admission was 7240 U/l, and later started to decline gradually. Other laboratory results such as urea, creatinine, alanine aminotransferase, and aspartate aminotransferase were also elevated significantly. Other laboratory tests like SGOT, SGPT returned to normal in subsequent investigations. However, Urea and Creatinine did not normalize in our patient.

As stated in the introduction, the early complications of rhabdomyolysis are hyperkalemia, hypocalcemia, elevated liver enzymes, cardiac dysrhythmias and cardiac arrest, while the late complications include acute kidney injury and DIC (disseminated intravascular coagulation).

In rhabdomyolysis, Dehydration, as well as aciduria, are salient contributing factors for AKI development [4]. Reduced blood supply to kidneys due to constriction of blood vessels to kidneys with decreased renal circulation, intraluminal cast formation, and direct heme protein-induced cytotoxicity are the main pathophysiology responsible for AKI development [7,8]. Long-term survival is close to 80%, among the patients with rhabdomyolysis and AKI. Most the patients with rhabdomyolysis-induced AKI recover renal function, although in this case AKI did not recover and the patient proceeded to require hemodialysis even after 1 month, pending biopsy of the kidney.

The risk of AKI is generally low in patients where the creatinine kinase levels were less than 5000 U/L on admission, though there have been rare instances of AKI developing with lower creatine kinase values less than 5000 U/L.

Acute kidney injury had developed in our patient at admission and the CK value of the patient was 7240 U/l. The CK value was elevated more than 5 times the normal value which is consistent with CK values of patients who developed AKI after rhabdomyolysis. Urea, and creatinine of the patient did not return to normal after appropriate treatment of early rehydration with saline, bicarbonate treatment, and even after 12 cycles of hemodialysis. Urine output of this patient upon presentation was normal and over the 7th day of his admission, the patient became oliguric. In a few days, Urine output gradually increased but the urea creatinine remained high.

In conclusion, this case review article emphasizes the importance of recognizing rhabdomyolysis early, after a suspected seizure episode even in the absence of red brown colored urine, to prevent potentially life-threatening, acute renal injury, which may lead to acute renal failure and even a complication that has high morbidity, the ESRD (end stage renal disease).

References

  1. Larbi EB. Drug-induced rhabdomyolysis. Ann Saudi Med. 1998;18:525-30.
  2. Grossman RA, Hamilton RW, Morse BM, et al. Nontraumatic rhabdomyolysis and acute renal failure. N Engl J Med. 1974;291:807-11.
  3. Mehlhorn AT, Strohm PC, Hausschildt O, et al. Seizure-induced muscle force can caused lumbar fracture. Acta Chir Orthop Traumatol Cech. 2007;74:202-5.
  4. Ward MM. Factors predictive of acute renal failure in rhabdomyolysis. Arch Intern Med. 1988;148:1553-7.
  5. Huerta-Alardin AL, Varon J, Marik PE. Bench-to-bedside review: Rhabdomyolysis: An overview for clinicians. Crit Care. 2005;9:158-69.
  6. Latham J, Campbell D, Nichols W, et al. Clinical inquiries. How much can exercise raise the creatine kinase level-and does it matter? J Fam Pract. 2008;57:545-7.
  7. Braun SR, Weiss FR, Keller AL, et al. Evaluation of the renal toxicity of heme pigments and their derivatives: A role in the genesis of acute tubular necrosis. J Exp Med. 1970;131:443-60.
  8. Bywaters EG, Beall D. Crush injuries with impairment of renal function. Br Med J. 1941;1:427-32.
  9. Gupta P, Singh VP, Chatterjee S, et al. Acute renal failure resulting from rhabdomyolysis following a seizure. Singapore Med J. 2010;51:e79-80.

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