Download presentation
Presentation is loading. Please wait.
Published byBriana Sanders Modified over 9 years ago
1
Leanna R. Miller, RN, MN, CCRN-CSC, PCCN-CMC, CEN, CNRN, CMSRN, NP Education Specialist LRM Consulting Nashville, TN
2
Objectives Identify the causes of rhabdomyolysis. Describe signs and symptoms of rhabdomyolysis. Utilizing a case study, identify management strategies of a patient with renal dysfunction resulting from rhabdomyolysis.
3
“Rhabdomyolysis was first reported in 1881, in the German literature” (Abbeele, Parker, 1985). “Rhabdomyolysis was first described in the victims of crush injury during the 1940- 1941 London, England, bombing raids of World War II” (Craig, 2006).
4
Rhabdomyolysis accounts for an estimated 8-15% of cases of acute renal failure. the overall mortality rate for patients with Rhabdomyolysis is approximately 5% Rhabdomyolysis is more common in males than in females may occur in infants, toddlers, and adolescents
5
disintegration of striated muscle results in the release of muscular cell constituents into the extracellular fluid and the circulation major component released is myoglobin
6
massive amounts of myoglobin are released the binding capacity of the plasma protein is exceeded myoglobin is then filtered by the glomeruli and reaches the tubules, where it may cause obstruction and renal dysfunction
7
syndrome characterized by muscle necrosis and the release of intracellular muscle constituents into the circulation creatine kinase (CK) levels are typically markedly elevated, and muscle pain and myoglobinuria may be present
8
severity of illness ranges from asymptomatic elevations in serum muscle enzymes to life-threatening disease associated with: extreme enzyme elevations electrolyte imbalances acute kidney injury
9
Rhabdomyolysis is the breakdown of muscle fibers, specifically of the sarcolemma of skeletal muscle, resulting in the release of muscle fiber contents (myoglobin) into the bloodstream.
10
The sarcolemma is the cell membrane of a muscle cell. The membrane is designed to receive and conduct stimuli Source: (Muscle Anatomy & Structure, 2007)
11
when muscle is damaged, a protein pigment - myoglobin is released into the bloodstream and filtered out of the body by the kidneys. broken down myoglobin may block the structures of the kidney, causing damage such as acute tubular necrosis or kidney failure. dead muscle tissue may cause a large amount of fluid to move from the blood into the muscle, leading to hypovolemic shock reduced blood flow to the kidneys.
13
may result from a large variety of diseases, TRAUMA, or toxic insults to skeletal muscle hereditary myopathies
14
Causes trauma burns compression syndrome infection seizures heat intolerance heat stroke
15
Causes vascular occlusion prolonged shock electrolyte disorders drugs (cocaine, alcohol, statins, amphetamine) low phosphate levels shaking chills
16
Clinical Manifestations muscle tenderness myalgias muscle swelling & weakness DIC color of urine
17
Additionally some possible symptoms include: −Overall fatigue −Joint pain −Seizures −Weight gain
18
Diagnosis an examination reveals tender or damaged skeletal muscles Creatine Phosphokinase (CK) levels are very high serum myoglobin test is positive serum potassium may be very high
19
serum CK begins to rise within 2 to 12 hours following the onset of muscle injury and reaches its maximum within 24 to 72 hours decline is usually seen within three to five days of cessation of muscle injury
20
CK has a serum half-life of about 1.5 days and declines at a relatively constant rate of about 40 to 50 percent of the previous day’s value patients whose CK does not decline as expected, continued muscle injury or the development of a compartment syndrome may be present
21
Diagnosis Urinalysis may reveal protein and be positive for hemoglobin without evidence of red blood cells on microscopic examination Urine myoglobin test is positive
22
Urine Myoglobin visible changes in the urine only occur once urine levels exceed from about 100 to 300 mg/dL can be detected by the urine dipstick at concentrations of only 0.5 to 1 mg/dL half-life of only two to three hours, much shorter than that of CK. rapidly excreted and metabolized to bilirubin, serum levels may return to normal within six to eight hours
23
Lab Values elevated muscle enzymes (CK) hyperkalemia hyperphosphatemia hypocalcemia
24
Complications Kidney damage Acute renal failure Hyperkalemia Cardiac arrest Disseminated Intravascular Coagulation Compartment syndrome
25
Treatment volume replacement treat electrolyte abnormalities protect renal perfusion alkalinization of urine fasciotomy
26
early and aggressive fluids (hydration) may prevent complications by rapidly remove myoglobin out of the kidneys. administer isotonic crystalloid fluids (Normal Saline or Lactated Ringer’s) give as much fluid as you would give a severely burned patient.
27
studies of patients with severe crush injuries resulting in Rhabdomyolysis suggest that the prognosis is better when prehospital personnel provide FLUID RESUCITATION!
28
medicines that may be prescribed include diuretics and sodium bicarbonate. hyperkalemia should be treated if present kidney failure should be treated as appropriate
29
if urinary flow is >20 mL/hour add mannitol to the intravenous alkaline solution providing an increase in urine output is demonstrated following a test dose suggested test dose is 60 mL of a 20 percent solution of mannitol administered intravenously over three to five minutes
30
if urine output increases by at least 30 to 50 mL/h above baseline levels in response to the test dose, 50 mL of 20 percent mannitol (1 to 2 g/kg per day [total, 120 g], may be given at a rate of 5 g/hour. mannitol is contraindicated in patients with oliguria
31
The outcome varies depending on the extent of kidney damage. Source: Silberber, 2007
33
Renal Failure Index (RFI) RFI = UNa x SCr/UCr Intrepretation RFI < 1 (prerenal failure) RFI > 1 (intrarenal failure)
34
Fraction Excreted Sodium (FENa) FE Na = U na X P Cr / P na X U cr x 100 Intrepretation FENa < 1 (prerenal failure) FENa > 1 (intrarenal failure)
35
Renal Failure Index (RFI) RFI = UNa x SCr/UCr Example RFI > 1 UNa>40 mEq/L FENa > 2-3% UCr/SCr<20
36
Renal Biomarkers Urine interleukin – 18 (IL – 18) Urine or blood NGAL neutrophil gelatinase – associated lipocalin Increase 24 to 48 hours earlier than creatinine
37
Intrinsic Diagnostics BUN/Creatinine ratio RFI/FENa urinalysis
38
Treatment underlying cause prevention on injury high risk patient hydration limit exposure
39
Management Principles maintain fluid balance manage hyperkalemia glucose & insulin sodium bicarbonate calcium gluconate albuterol
40
Clinical Manifestations hyperkalemia hypocalcemia hypermagnesemia hyperphosphatemia acid – base imbalance
41
hypocalcemia occurs in up to two- thirds of patients with significant rhabdomyolysis increase in serum phosphate deposition of calcium phosphate into injured muscle decreased bone responsiveness to parathyroid hormone
42
Management Principles control hypertension in presence of encephalopathy bicarbonate for severe acidosis (pH < 7.2) manage anemia
43
Renal Replacement Therapies
44
Treatment Replacement Therapies acidosis HCO 3 < 10 mEq/L K + > 6.5 mEq/L need high protein diet deteriorating
45
Treatment: Types hemodialysis continuous renal replacement therapy
46
Treatment fluid balance anticoagulation prevent clotting prevent blood loss ultrafiltration
47
Case Study 20 – year old male with friends “doing drugs – cocaine” police break up party – male runs from police but collaspes – states legs became so weak that he fell admitted to ED – lower extremity weakness and severe pain in legs
48
Case Study Serum ElectrolytesABGs Na 141 K 6.7 Cl 104 CO 2 7 Creatinine 4.5 BUN 20 Ca 5.0 Mg 2.0 PO 4 11.2 pH 7.11 PaCO 2 27 PaO 2 97 SaO 2 98% HCO 3 7
49
Case Study Serum EnzymesHematology ValuesClotting Profile CK 4,780 LDH 812 Hct 30 WBC 18,400 PT 28 PTT >180 Platelets 80,000
50
Case Study UrinalysisSedimentUrine Chemistries Color Reddish brown SG 1.008 pH 5.0 RBC 0-1 WBC 4-5 Casts granular & epithelial Urine Na 42 Urine Osm 280
51
wide variety of situations that cause rhabdomyolysis focus is fluid resuscitation and surgical intervention if compartment syndrome develops ARF is a common consequence – treat as you would any type of intrinsic ARF
Similar presentations
© 2025 SlidePlayer.com. Inc.
All rights reserved.