<?xml version="1.0" encoding="UTF-8"?><!DOCTYPE article  PUBLIC "-//NLM//DTD Journal Publishing DTD v3.0 20080202//EN" "http://dtd.nlm.nih.gov/publishing/3.0/journalpublishing3.dtd"><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" dtd-version="3.0" xml:lang="en" article-type="research article"><front><journal-meta><journal-id journal-id-type="publisher-id">OJIM</journal-id><journal-title-group><journal-title>Open Journal of Internal Medicine</journal-title></journal-title-group><issn pub-type="epub">2162-5972</issn><publisher><publisher-name>Scientific Research Publishing</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.4236/ojim.2023.131004</article-id><article-id pub-id-type="publisher-id">OJIM-123485</article-id><article-categories><subj-group subj-group-type="heading"><subject>Articles</subject></subj-group><subj-group subj-group-type="Discipline-v2"><subject>Medicine&amp;Healthcare</subject></subj-group></article-categories><title-group><article-title>
 
 
  Management of Rhabdomyolysis and Acute Renal Failure Following Strenuous Exercise in Young Adult: A Case Report
 
</article-title></title-group><contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Musab</surname><given-names>Eltayeb</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="corresp" rid="cor1"><sup>*</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Amna</surname><given-names>Sirag</given-names></name><xref ref-type="aff" rid="aff2"><sup>2</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Hisham</surname><given-names>Alamin</given-names></name><xref ref-type="aff" rid="aff3"><sup>3</sup></xref><xref ref-type="corresp" rid="cor1"><sup>*</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Alnour</surname><given-names>Elagib</given-names></name><xref ref-type="aff" rid="aff4"><sup>4</sup></xref><xref ref-type="corresp" rid="cor1"><sup>*</sup></xref></contrib></contrib-group><aff id="aff1"><addr-line>Department of Rheumatology, University Hospital Limerick, Limerick, Ireland</addr-line></aff><aff id="aff2"><addr-line>Internal Medicine, Sudan Medical Specialization Board, Khartoum, Sudan</addr-line></aff><aff id="aff4"><addr-line>Internal Medicine Department, Karary University, Omdurman, Sudan</addr-line></aff><aff id="aff3"><addr-line>Department of Internal Medicine, National Ribat University, Khartoum, Sudan</addr-line></aff><pub-date pub-type="epub"><day>02</day><month>02</month><year>2023</year></pub-date><volume>13</volume><issue>01</issue><fpage>23</fpage><lpage>31</lpage><history><date date-type="received"><day>15,</day>	<month>January</month>	<year>2023</year></date><date date-type="rev-recd"><day>26,</day>	<month>February</month>	<year>2023</year>	</date><date date-type="accepted"><day>1,</day>	<month>March</month>	<year>2023</year></date></history><permissions><copyright-statement>&#169; Copyright  2014 by authors and Scientific Research Publishing Inc. </copyright-statement><copyright-year>2014</copyright-year><license><license-p>This work is licensed under the Creative Commons Attribution International License (CC BY). http://creativecommons.org/licenses/by/4.0/</license-p></license></permissions><abstract><p>
 
 
  Introduction: Rhabdomyolysis is severe and life threating condition in which skeletal muscles are damaged by dissolution of striped muscles. Acute kidney injury (AKI) has been widely reported (13% - 50%) as a complication of Rhabdomyolysis in which the main pathophysiological mechanisms are intra-renal vasoconstriction, intraluminal cast formation (Tamm-Horsefall) and direct myoglobin toxicity. In this report we are going to describe the management of Acute Kidney Injury due to Rhabdomyolysis that is not responding to vigorous rehydration. 
  Objective: Reporting about acute renal failure induced by Rhabdomyolysis due to Excessive Exercise and dehydration in young patient. 
  Case Report: A 20 years male came to the outpatient clinic complaining of sever lower limb pain, back pain and vomiting. He was anuric and hypertensive (BP = 150/90 mmHg) with serum creatinine and urea levels of 15.72 mg/dl and 235 mg/dl, respectively. The diagnosis was based on the laboratory finding of creatine kinase = 3127 IU/l. The patient, then, has been referred to the emergency department. The Management plan was based on two arms: Emergency Management with Urgent Hemodialysis for AKI and high fluid replacement therapy. Patient started to recover after three hemodialysis sessions but the peak of recovery was noted after starting manual fluid replacement therapy with a target urine output of greater than 2 ml/kg, a urine pH of greater than 6. Manual fluid replacement therapy consisted of loop diuretics, intravenous fluids and intravenous sodium bicarbonate 1.26%. Full recovery was noted after one month of hospital admission with inpatient care and regular follow-up. A follow-up after one month has been set to assess the patient progression and monitor his kidney functions. 
  Relevance and Impact: Home messages and lessons are; Firstly, young adults are vulnerable to Rhabdomyolysis, second, the diagnosis of Rhabdomyolysis can be made on the clinical bases but a confirmatory laboratory test of Creatine Kinase is mandatory, and lastly’ acute kidney injury needs to be treated urgently. Also, reducing the risk of infection is one of the management objectives to achieve recovery.
 
</p></abstract><kwd-group><kwd>Rhabdomyolysis</kwd><kwd> Acute Kidney Injury</kwd><kwd> Strenuous Exercise</kwd><kwd> Case Report</kwd><kwd> Manual Fluid Replacement Therapy</kwd></kwd-group></article-meta></front><body><sec id="s1"><title>1. Introduction</title><p>This Rhabdomyolysis is a syndrome characterized by muscle necrosis followed by release of intracellular muscle contents into the circulation. The intracellular muscle contents which are released after muscle injury include: Massive plasma myoglobin levels exceeds protein binding (of haptoglobin).</p><p>It has numerous causes: use of drugs, muscles trauma, exposure to toxins, infections, hyperthermia, seizures and electrolytes abnormalities leading to cell lysis through ischemia and acidosis [<xref ref-type="bibr" rid="scirp.123485-ref1">1</xref>] - [<xref ref-type="bibr" rid="scirp.123485-ref7">7</xref>] .</p><p>Strenuous exercise may lead to disintegration of striated muscles, resulting in release of muscles constitutes into extracellular fluid and circulation. This consequently cause pigment-nephropathy and AKI [<xref ref-type="bibr" rid="scirp.123485-ref8">8</xref>] [<xref ref-type="bibr" rid="scirp.123485-ref9">9</xref>] . AKI has been reported to complicate 13% - 50% with average of 33% cases of Rhabdomyolysis [<xref ref-type="bibr" rid="scirp.123485-ref1">1</xref>] [<xref ref-type="bibr" rid="scirp.123485-ref10">10</xref>] . The pathophysiology of AKI induced by Rhabdomyolysis is: intra-renal vasoconstriction, direct tubular toxicity and tubular obstruction by Tamm-Horsfall protein containing casts all of which are precipitated by presence of myoglobin [<xref ref-type="bibr" rid="scirp.123485-ref1">1</xref>] .</p><p>The Classic Triad of Rhabdomyolysis (Myalgia, Generalized weakness and Darkened urine) is only seen in 50% of patient and it is less common in Children [<xref ref-type="bibr" rid="scirp.123485-ref11">11</xref>] . Physical examination patient may have muscular pain and tenderness, decreased muscle strength, soft tissue swelling and skin changes consistent with pressure necrosis. The most commonly involved muscle groups in adults include: the calves and the lower back. Chest, back and calf pain often mimics other common conditions such as deep vein thrombosis or angina. Peripheral pulses might be intact even after evolving of compartment syndrome because it is very late sign. Even if the patient is lacking the classic history, physical examination findings or both, diagnosis of Rhabdomyolysis should not be rolled out if the suspicion is based on clinical scenario and an appropriate laboratory evaluation should be performed to diagnose muscle damaged and organ dysfunction [<xref ref-type="bibr" rid="scirp.123485-ref4">4</xref>] .</p><p>Diagnosis of Rhabdomyolysis can be confirmed using certain laboratory studies [<xref ref-type="bibr" rid="scirp.123485-ref12">12</xref>] . For Muscle injury the most reliable and sensitive indicator is creatine kinase (CK). It presents in serum immediately after muscle injury, rise within 12 hours and reach a peak in 24 - 36 hours, and decrease at a rate of 30% - 40% per day [<xref ref-type="bibr" rid="scirp.123485-ref13">13</xref>] . The serum half-life of CK is approximately 36 hours. CK Levels decline 3 - 5 days after resolution of Muscle injury [<xref ref-type="bibr" rid="scirp.123485-ref12">12</xref>] . Renal profile should be performed. Despite being a diagnostic marker for Rhabdomyolysis, initial creatine kinase levels do not predict mortality. However, creatinine initial levels are related to progression to acute renal injury and mortality at 30 days [<xref ref-type="bibr" rid="scirp.123485-ref14">14</xref>] . Other Routine investigations should be performed such as Complete Blood Count, urine analysis and Serum Chemistries such Glucose, Liver function tests and Potassium to detect complications.</p><p>The complications of Rhabdomyolysis beside AKI are: Electrolyte abnormalities such as hyperkalemia, hypocalcemia and hypoalbuminemia, Compartment syndrome and disseminated intravascular coagulation (DIC) [<xref ref-type="bibr" rid="scirp.123485-ref4">4</xref>] [<xref ref-type="bibr" rid="scirp.123485-ref12">12</xref>] [<xref ref-type="bibr" rid="scirp.123485-ref15">15</xref>] .</p><p>There are few publications on exercise induced Rhabdomyolysis leading to AKI exist in the literature. After taking Clearance and patient consent, we are reporting exercise induced Rhabdomyolysis leading to AKI case of 20 years old male.</p></sec><sec id="s2"><title>2. Case Report</title><sec id="s2_1"><title>2.1. Patient Information’s and Clinical Findings</title><p>A 20 years male was exercising vigorously in a hot and humid weather without keeping a good hydration. 24 hours after his vigorous exercise he came to the outpatient clinic complaining of vomiting everything he eats, lower limbs pain (Myalgia), back pain and he was unable to pass urine. He was referred from the outpatient clinic with a provisional diagnosis of Rhabdomyolysis to the emergency department. The vomiting was following any oral intake. The patient vomited twice before presenting to the outpatient clinic and he was fasting because he did not want to vomit. The patient is not known to have any chronic illnesses (Diabetes Mellitus, Hypertension, Asthma etc.). The patient is not known to have any allergies. He had no history of hospital admission, surgical operations nor blood transfer. The patient is originally from Sennar a state that is around 300 km away to the north of Khartoum the capital of Sudan. There is a family history of DM and hypertension. On examination the patient looked unwell, he was febrile (38˚C), His Blood pressure was 151/88 mmHg and his pulse rate was 82 b/min (<xref ref-type="table" rid="table1"><xref ref-type="table" rid="table">Table </xref>1</xref>). He had tender back and lower limbs. No other abnormalities were detected. The following investigation was requested: Creatine Phospho-kinase, Serum phosphorus, Serum Calcium, Serum Uric Acid, Renal function test, complete blood picture and blood film for malaria. The patient was admitted to the emergency ward and planned for the following: urine input/output chart, vigorous fluid replacement therapy with rate of 125 ml/hour and nephrology unit consultation. Results of investigation were available in the 2<sup>nd</sup> day of admission (<xref ref-type="table" rid="table2"><xref ref-type="table" rid="table">Table </xref>2</xref>). The diagnosis has been confirmed in the 4<sup>th</sup> day of admission with the CPK level is 3127 IU/L. The nephrology unit decided 3 urgent hemodialysis sessions for the patient in 2<sup>nd</sup> day of admission. Management</p><table-wrap id="table1" ><label><xref ref-type="table" rid="table1"><xref ref-type="table" rid="table">Table </xref>1</xref></label><caption><title> Showing vital signs during hospital stay</title></caption><table><tbody><thead><tr><th align="center" valign="middle"  rowspan="2"  >Days</th><th align="center" valign="middle"  colspan="3"  >Vitals</th><th align="center" valign="middle" ></th></tr></thead><tr><td align="center" valign="middle" >Blood pressure</td><td align="center" valign="middle" >Pulse rate</td><td align="center" valign="middle" >Respiratory rate</td><td align="center" valign="middle" >Temperature</td></tr><tr><td align="center" valign="middle" >1st day 2nd day 3rd day 4th day 5th day 6th day 7th day 8th day 9th day 10th day 11th day 12th day 13th day 14th day 15th day 16th day 17th day 18th day 19th day 20th day 21st day 22nd day 23rd day 24th day 25th day 26th day 27th day 28th day</td><td align="center" valign="middle" >151/88 150/90 130/70 170/90 160/90 180/110 160/90 150/100 160/80 140/90 140/80 170/110 130/70 155/80 140/80 130/90 150/90 - 130/70 - - 90/70 130/80 - - 140/80 - 140/80</td><td align="center" valign="middle" >82 80 70 68 80 96 88 86 116 67 94 97 - 80 82 88 72 - 74 76 - 110 90 - - 94 - 82</td><td align="center" valign="middle" >22 20 18 21 24 20 21 26 32 19 23 20 25 22 22 20 22 - - - - 22 20 - - 22 - 21</td><td align="center" valign="middle" >38 36.5 37.3</td></tr></tbody></table></table-wrap><p>with 3 liters of Normal Saline continued along with Ranitidine. After the 2<sup>nd</sup> dialysis session the patient blood pressure started to rise BP = 150/90 mmHg (<xref ref-type="table" rid="table1"><xref ref-type="table" rid="table">Table </xref>1</xref>). Amlodipine 5 mg had been added to the management plan. After the 3<sup>rd</sup> dialysis session the blood pressure was recorded was really high reaching = 170/90 mmHg (<xref ref-type="table" rid="table1"><xref ref-type="table" rid="table">Table </xref>1</xref>). On the 5<sup>th</sup> day of admission the patient completed the 3 urgent dialysis sessions of 9 hours and half with 250 blood flow and ultrafiltration of 2000. The blood pressure was still high with 160/90 and the amlodipine had been increased to 10 mg. The creatine level was 9.2 mg/dl and urea was 90 mg/dl (<xref ref-type="table" rid="table2"><xref ref-type="table" rid="table">Table </xref>2</xref>). The nephrology unit decided to continue the dialysis with a 4<sup>th</sup></p><table-wrap id="table2" ><label><xref ref-type="table" rid="table2"><xref ref-type="table" rid="table">Table </xref>2</xref></label><caption><title> Showing most important the blood investigations during hospital stay</title></caption><table><tbody><thead><tr><th align="center" valign="middle"  rowspan="2"  >Investigations</th><th align="center" valign="middle" ></th><th align="center" valign="middle"  colspan="3"  >Days</th><th align="center" valign="middle" ></th><th align="center" valign="middle" ></th><th align="center" valign="middle" ></th><th align="center" valign="middle" ></th><th align="center" valign="middle" ></th><th align="center" valign="middle" ></th><th align="center" valign="middle" ></th></tr></thead><tr><td align="center" valign="middle" >2nd</td><td align="center" valign="middle" >3rd</td><td align="center" valign="middle" >4th</td><td align="center" valign="middle" >5th</td><td align="center" valign="middle" >9th</td><td align="center" valign="middle" >13th</td><td align="center" valign="middle" ></td><td align="center" valign="middle" ></td><td align="center" valign="middle" ></td><td align="center" valign="middle" ></td><td align="center" valign="middle" ></td></tr><tr><td align="center" valign="middle" >CPK Urea Creatinine S. Magnesium S. Phosphorus S. Potassium S. Calcium S. Sodium WBC PLT HB Glucose T. Protein Albumin AST ALT PTT INR BFFM Uric acid</td><td align="center" valign="middle" >--- 235 15.7 2.7 0.2 3.6 8.4 128 7.6 344 11.6 195 4.7 2.3 295 341 −ve</td><td align="center" valign="middle" >--- 204 14.8 3.9 134 100</td><td align="center" valign="middle" >3127 137 12.09 4.1 147 98 7.39</td><td align="center" valign="middle" >--- 90 9.20 4.1 139 7.4 306 10.1 −ve</td><td align="center" valign="middle" >--- 94 10.67 3.3 144 102</td><td align="center" valign="middle" >166 86 7.62 3.0 145 106</td><td align="center" valign="middle" >93 55 3.2 3.8 147 98</td><td align="center" valign="middle" >95 4.1 2.7 143 93</td><td align="center" valign="middle" >62 2.61 3.0 144 9.0 500 9.1</td><td align="center" valign="middle" >48 0.8 3.7 118</td><td align="center" valign="middle" >28 1.1 4.0 135 6.5 461 9.7 138</td></tr></tbody></table></table-wrap><p>session. The fluid input/output chart was not established and patient started to develop puffiness of the face, the patient was still complaining of vomiting and injectable Ondansetron 8 mg once daily had been added to the management plan instead of the pantoprazole 40 mg and the ranitidine 25 mg. On the 6<sup>th</sup> day of admission the fluid input/output chart had been established indicating a positive difference in the input and output chart of 1420 ml not being cleared from the body (<xref ref-type="table" rid="table3"><xref ref-type="table" rid="table">Table </xref>3</xref>). On the 7<sup>th</sup> day of admission the patient developed generalized edema and puffiness of the face. The input/output chart indicated a positive difference of 1500 ml (<xref ref-type="table" rid="table3"><xref ref-type="table" rid="table">Table </xref>3</xref>). Furosemide had been added after several discussion with the nephrology unit. Antihistamine and Hydrocortisone trial had been initiated to guard against hypersensitivity reaction to Amlodipine. On the 8<sup>th</sup> day of admission the patient developed fever temperature was 37.3˚C and shortness of breath with respiratory rate of 26 cycle/min (<xref ref-type="table" rid="table1"><xref ref-type="table" rid="table">Table </xref>1</xref>). Arterial blood gases test was obtained (<xref ref-type="table" rid="table4"><xref ref-type="table" rid="table">Table </xref>4</xref>) and the balance in the 8<sup>th</sup> day of admission was 2550 ml positive balance (<xref ref-type="table" rid="table3"><xref ref-type="table" rid="table">Table </xref>3</xref>). Ceftriaxone 1 gm intravenously twice a day and paracetamol one gram intravenously as needed had been added. The furosemide had been stopped based on the recommendation of the nephrology</p><table-wrap id="table3" ><label><xref ref-type="table" rid="table3"><xref ref-type="table" rid="table">Table </xref>3</xref></label><caption><title> <xref ref-type="table" rid="table">Table </xref>demonstrates the input and output chart during important hospital milestones</title></caption><table><tbody><thead><tr><th align="center" valign="middle"  rowspan="2"  >Days</th><th align="center" valign="middle" ></th><th align="center" valign="middle"  colspan="3"  >Input/Output Chart</th><th align="center" valign="middle" ></th><th align="center" valign="middle" ></th><th align="center" valign="middle" ></th></tr></thead><tr><td align="center" valign="middle" >Oral intake</td><td align="center" valign="middle" >Intravenous</td><td align="center" valign="middle" >Total Input</td><td align="center" valign="middle" >Urine output</td><td align="center" valign="middle" >Vomiting</td><td align="center" valign="middle" >Total Output</td><td align="center" valign="middle" >Balance</td></tr><tr><td align="center" valign="middle" >6th 7th 8th 9th 11th</td><td align="center" valign="middle" >350 ml 100 ml 450 ml 1700 ml 1800 ml</td><td align="center" valign="middle" >2220 ml 3000 ml 3500 ml 3100 ml 2500 ml</td><td align="center" valign="middle" >2570 ml 3100 ml 3950 ml 4800 ml 4300 ml</td><td align="center" valign="middle" >800 ml 1500 ml 1200 ml 1900 ml 3500 ml</td><td align="center" valign="middle" >250 ml 100 ml 200 ml 200 ml 0 ml</td><td align="center" valign="middle" >1150 ml 1600 ml 1400 ml 2100 ml 3500 ml</td><td align="center" valign="middle" >1420 ml 1500 ml 2550 ml 2700 ml 800 ml</td></tr></tbody></table></table-wrap><table-wrap id="table4" ><label><xref ref-type="table" rid="table4"><xref ref-type="table" rid="table">Table </xref>4</xref></label><caption><title> Arterial blood gas upon admission</title></caption><table><tbody><thead><tr><th align="center" valign="middle" >ABG</th><th align="center" valign="middle" >Results</th></tr></thead><tr><td align="center" valign="middle" >pH pCO<sub>2</sub> pO<sub>2</sub> HCO−1 3 SpO<sub>2</sub> Na<sup>+</sup> K<sup>+</sup> Lactic acid Anion gap Hb</td><td align="center" valign="middle" >7.399 27.7 mmHg 126 mmHg 17.3 mmol/l 98.9% 137 mmol/l 3.5 mmo/l 1.1 mmol/l 12.1 9.9 g/dl</td></tr></tbody></table></table-wrap><p>unit. After thoroughly discussing the case with the nephrology unit the fluids had been shifted to fluid therapy with bicarbonate. The plan of fluids was as following: 4 liters of fluids divided; into 1 liter of Dextrose 5% with Sodium bicarbonate 75 ml, alternating with 1 liter of Normal Saline every 6 hours. On the 9<sup>th</sup> day BP was 160/80 mmHg, fever has stopped and vomiting decreased to 2 times per day RR was 32 cycle/minute (<xref ref-type="table" rid="table1"><xref ref-type="table" rid="table">Table </xref>1</xref>). Hypersensitivity drugs had been stopped and fluid balance was positive with 2700 ml and the urine output increasing to 1900 ml per day (<xref ref-type="table" rid="table3"><xref ref-type="table" rid="table">Table </xref>3</xref>). The high fluids therapy with bicarbonate showed tremendous improvement in the renal function test (<xref ref-type="table" rid="table2"><xref ref-type="table" rid="table">Table </xref>2</xref>). The patient underwent the 4<sup>th</sup> dialysis session in the 11<sup>th</sup> day of admission. After the hemodialysis session and fluid therapy, the facial swelling and puffiness has subsided slightly. The fluid and bicarbonate therapy continued and Ondansetron had been increased to be administered twice a day and promethazine hydrochloride to be administered if needed. The facial swelling and urine output improved as the balance had reach almost positive 800 ml (<xref ref-type="table" rid="table3"><xref ref-type="table" rid="table">Table </xref>3</xref>). CPK was done in the 13<sup>th</sup> day of admission and found to be 166 IU/L. The renal function test was improving with combination of fluid therapy and bicarbonate Sodium (<xref ref-type="table" rid="table2"><xref ref-type="table" rid="table">Table </xref>2</xref>). Blood pressure started to be maintained with Amlodipine 10 mg daily (<xref ref-type="table" rid="table1"><xref ref-type="table" rid="table">Table </xref>1</xref>). On the 17<sup>th</sup> day of admission CPK found to be 93 IU/L. On the 22<sup>st</sup> day of admission the patient had low potassium in his RFT as he did not establish oral feeding well due to his fear of vomiting. KCL 30 mmol had been added to his fluid therapy three times per day (Total of 1.5 L of NS) and bicarbonate sodium had been stopped. Regular Ondansetron had been shifted to be administered if there was vomiting and antihypertensive had been stopped. On the 22<sup>th</sup> day of the patient started to develop fever, chills and shivering. TWBCs was high (<xref ref-type="table" rid="table2"><xref ref-type="table" rid="table">Table </xref>2</xref>) and he vomited twice his blood pressure was 90/60 mmHg (<xref ref-type="table" rid="table1"><xref ref-type="table" rid="table">Table </xref>1</xref>). Urine catheter had been inserted for more than 21 days which led to UTI. Antibiotics had been changed to vancomycin and cefepime with renal impairment consideration. Fluids had been increased to 1 liter and 30 mmol KCL 3 times a day. Catheter had been removed. On the 26<sup>th</sup> day of admission the patient RFT has normalized and he started full oral intake (<xref ref-type="table" rid="table2"><xref ref-type="table" rid="table">Table </xref>2</xref>). Urinary Catheter had been removed 2 days previously and dialysis catheter planned to be removed after discharge. On the 28<sup>th</sup> day of admission patient discharge decision has been taken by a joint meeting between Medicine unit and nephrology unit. A follow-up after 1 month was scheduled. The follow-up will be mainly to assess the kidneys function and to measure the blood pressure. The prognosis after full recovery from the Acute Kidney injury is promising.</p></sec><sec id="s2_2"><title>2.2. Discussion</title><p>This case needed close monitoring and multidisciplinary team approach as the internal medicine joined effort with the nephrology unit and nursing staff of the general ward. The integration of manual fluid replacement and bicarbonate usage was new to all nursing and junior doctors as it is not used regularly.</p><p>Strengths of this case included the early diagnosis of the case has leaded to prompt management. A strong support of the diagnosis was the CK levels that were tested very early after the presentation was which was very high with more than 3000 (<xref ref-type="table" rid="table2"><xref ref-type="table" rid="table">Table </xref>2</xref>). One of the main limitations was in-spite of the early diagnosis of Rhabdomyolysis, Acute kidney failure which has responded to hemodialysis only. A major limitation was the catheter associated infection which has slowed down the recovery and increased inpatient stay. The urinary catheter has stayed for more than 14 days which indicated poor documentation and handover.</p><p>Relevant literature and case reports:</p><p>The presentation was almost typical in this case with exception of red urine. The patient was not able to pass urine in the presentation. Usually the presentation of the Rhabdomyolysis patient is muscle pain and red urine [<xref ref-type="bibr" rid="scirp.123485-ref1">1</xref>] . The severity of this is demonstrated by the presentation of the patient with acute kidney injury which a sign of the severity of the case [<xref ref-type="bibr" rid="scirp.123485-ref16">16</xref>] . There are cases that have been reported with higher CK levels but it has not reach the severity of this case with acute kidney injury [<xref ref-type="bibr" rid="scirp.123485-ref16">16</xref>] . The management of this case is considered the classic management of any patient presenting with acute kidney injury induced by Rhabdomyolysis [<xref ref-type="bibr" rid="scirp.123485-ref6">6</xref>] .</p><p>Take home messages are fluid replacement should not be delayed. The invasive devices should be checked their duration should be documented in the patient chart and files. The earlier removal of invasive devices should be considered if deemed appropriate as hospital acquired infection is always expensive in terms of hospital stay and financial burden.</p><p>The patient consent has been taken from the patient himself and the case report has been discussed with him and the importance of the case report has been explained too.</p></sec><sec id="s2_3"><title>2.3. Conclusion</title><p>Rhabdomyolysis can be expected in young adults especially after strenuous exercise. The patient should be treated promptly as multi-organ failure is a complication associated with the delay of management. The manual fluid therapy should be initiated immediately and compartment syndrome management should be avoided as it can delay the recovery, though, it should not be delayed if needed.</p></sec></sec><sec id="s3"><title>Conflicts of Interest</title><p>The authors declare no conflicts of interest regarding the publication of this paper.</p></sec><sec id="s4"><title>Cite this paper</title><p>Eltayeb, M., Sirag, A., Alamin, H. and Elagib, A. (2023) Management of Rhabdomyolysis and Acute Renal Failure Following Strenuous Exercise in Young Adult: A Case Report. Open Journal of Internal Medicine, 13, 23-31. https://doi.org/10.4236/ojim.2023.131004</p></sec></body><back><ref-list><title>References</title><ref id="scirp.123485-ref1"><label>1</label><mixed-citation publication-type="other" xlink:type="simple">Bosch, X., Poch, E. and Grau, J.M. (2009) Rhabdomyolysis and Acute Kidney Injury. 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