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treatment of hepatic encephalopathy is usually based on correcting the precipitating
factor. In this patient, the precipitating factor was the increased production of
ammonia in the gut from the bacteria due to the bleeding gastric ulcer. In general,
rifaximin and lactulose are used as rst-line pharmacotherapy for hepatic encephalopathy [3]. Lactulose is a synthetic disaccharide laxative that decreases the absorption of ammonia by acidifying the gut. This results in the conversion of ammonia to
ammonium (NH
+
) which is excreted in the feces, instead of being reabsorbed [3].
4
Rifaximin is a broad-spectrum oral antibiotic that kills ammonia-producing intestinal bacteria, resulting in less ammonia being produced [2].
Conclusion
Patients presenting with cognitive impairment and confusion with suspected liver
cirrhosis should be evaluated for hepatic encephalopathy. A thorough diagnostic
workup with precise laboratory investigation and imaging modalities should be conducted to rule out any other causes of encephalopathy. Hepatic encephalopathy is
observed in more than 70% of patients with liver cirrhosis, and the accompanying
symptoms are usually reversible [2, 10]. As discussed above, proper investigations
and correct examination are essential to prevent misdiagnosis and further
complications.
References
1. Wijdicks EF. Hepatic encephalopathy. N Engl J Med. 2016;375(17):1660–70. https://doi.
org/10.1056/NEJMra1600561.
2. Patidar KR, Bajaj JS.Covert and overt hepatic encephalopathy: diagnosis and management.
Clin Gastroenterol Hepatol. 2015;13(12):2048–61. https://doi.org/10.1016/j.cgh.2015.06.039.
3. Gundling F, Zelihic E, Seidl H, Haller B, Umgelter A, Schepp W, Dodt C.How to diagnose
hepatic encephalopathy in the emergency department. Ann Hepatol. 2013;12(1):108–14.
4. Quero Guillén JC, Groeneweg M, Jiménez Sáenz M, Schalm SW, Herrerías Gutiérrez JM.Is it
a medical error if we do not screen cirrhotic patients for minimal hepatic encephalopathy? Rev
Esp Enferm Dig. 2002;94(9):544–57.
5. Weissenborn K.Hepatic encephalopathy: denition, clinical grading and diagnostic principles.
Drugs. 2019;79(Suppl 1):5–9. https://doi.org/10.1007/s40265- 018- 1018- z.
6. Rose CF, Amodio P, Bajaj JS, Dhiman RK, Montagnese S, Taylor-Robinson SD, Vilstrup H,
Jalan R.Hepatic encephalopathy: novel insights into classication, pathophysiology and therapy. J Hepatol. 2020;73(6):1526–47. https://doi.org/10.1016/j.jhep.2020.07.013.
7. Rudler M, Weiss N, Bouzbib C, Thabut D.Diagnosis and management of hepatic encephalopathy. Clin Liver Dis. 2021;25(2):393–417. https://doi.org/10.1016/j.cld.2021.01.008.
8. King Faisal Specialist Hospital & Research Centre, 0000 (2022).
9. Elsaid MI, Rustgi VK. Epidemiology of hepatic encephalopathy. Clin Liver Dis.
2020;24(2):157–74. https://doi.org/10.1016/j.cld.2020.01.001.
10. Said VJ, Garcia-Trujillo E.Beyond lactulose: treatment options for hepatic encephalopathy.
Gastroenterol Nurs. 2019;42(3):277–85. https://doi.org/10.1097/SGA.0000000000000376.
Chapter 16
A Case ofMisdiagnosis ofRhabdomyolysis
MohammadJ.Ghosheh
Learning Objectives
By the end of this presentation, the clinician should be able to:
1. Recite the clinical presentation of rhabdomyolysis and its variations in clinical
practice.
2. Discuss how to diagnose rhabdomyolysis in the emergency department and
know what the most appropriate investigations are.
3. Enumerate the different causes of rhabdomyolysis and the complications associated with it.
4. Recite the pathophysiology of rhabdomyolysis and apply the knowledge
clinically.
5. Explain how to avoid misdiagnosing rhabdomyolysis to facilitate a better treatment approach to reduce complications and get better outcomes.
Introduction
Rhabdomyolysis is a clinical syndrome that results in the breakdown of skeletal
muscle. The destruction of the muscle tissue results in the release of intracellular
components into the bloodstream [1]. The intracellular components such as myoglobin, creatinine, and potassium that get released are primarily responsible for the
symptoms observed in rhabdomyolysis. The acute tubular necrosis and intrinsic
acute kidney injury that occurs in patients with rhabdomyolysis are a result of the
released myoglobin and creatinine kinase into the bloodstream, directly causing
obstruction of the intrinsic tubules and pigment nephropathy. Potassium and lactic
M. J. Ghosheh (*)
Al-Faisal University College of Medicine, Riyadh, Saudi Arabia
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
H. Tohid et al. (eds.), The Misdiagnosis Casebook in Clinical Medicine,
https://doi.org/10.1007/978-3-031-28296-6_16
105
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M. J. Ghosheh
Table 16.1
Traumatic Non-traumatic
Crush injury Ischemic necrosis
Prolonged immobilization Drug-induced
Overexertion Infections
Heat stroke Autoimmune
Electrical injury Intoxication
Categories and causes of rhabdomyolysis
acid are similarly released into the bloodstream, and their increased concentrations
consequently result in fatal cardiac arrhythmias and metabolic acidosis, respectively. Crush syndrome due to crush injury from trauma can cause hypovolemia and
shock, both resultantly contributing to further kidney injury and azotemia. A classic
diagnostic nding that is found specically in acute kidney injury associated with
myoglobinuria is the presence of blood on urine dipstick in the absence of red blood
cells in the urine sediment. Prolonged untreated rhabdomyolysis can result in serious life-threatening complications such as kidney failure, compartment syndrome,
and fatal arrhythmias. Therefore, an accurate diagnosis of rhabdomyolysis and its
management all in a timely manner is necessary.
The causes of rhabdomyolysis can vary signicantly and can present differently
depending on the cause. It is essential to understand and distinguish the different
causes of rhabdomyolysis and appreciate the different ways they can present.
The causes of rhabdomyolysis can be divided into two main categories as seen in
Table16.1 [2–4].
Clinical Case Presentation
A 26-year-old lady was admitted to the emergency department due to generalized
muscle pain. She has recently started working out at the gym a total of 4 hours every
day and eats a well-balanced diet.
She has a known medical history of recurrent kidney stones and urinary tract
infections. She takes no medications, except for when she was hospitalized for a
urinary tract infection 6 months ago. She is single and does not smoke and only
drinks alcohol on occasions. She has no signicant family history. General physical
examination shows diffuse tenderness on palpation of both her arms and legs.
Neurological examination is normal, and the patient is oriented to place, time, and
person. She was discharged home on painkillers and was advised to refrain from
exercising until her symptoms subsided. Later that day the patient was readmitted to
the emergency department with worsening of her symptoms, vomiting, and blood in
her urine. Her labs are shown below (Tables 16.2 and 16.3) [5].
16 A Case ofMisdiagnosis ofRhabdomyolysis
107
Table 16.2 Patient’s
vital signs
Table 16.3 Patient’s laboratory results
Parameter Results Reference range
Hemoglobin 12.4 g/dL 12.0–16.0
Hematocrit 42% 36%–46%
ESR 22 0–20
CRP 4 <10
Platelet count 250,000/mm
Leukocyte count 6900/mm
Creatinine 1.8 0.6–1.2
BUN 27 7–18
Creatine kinase (CK) 5600 10–70
Lactate dehydrogenase 322 45–200
Sodium 142 136–146
Potassium 6.8 3.5–5.0
Phosphate 5.8 3.0–4.5
Calcium 7.8 8.4–10.2
Chloride 114 95–105
Bicarbonate 18 22–28
Urinalysis Results Reference range
Blood 3+ Negative
WBC 1–2 0–5 per high-power eld
Protein 1+ Negative
RBC N/A 0–4 per high-power eld
Nitrite Negative Negative
Ketone Negative Negative
3
Parameters Results
Blood pressure 124/76 mmHg
Heart rate 67
Temperature (Celsius) 37.8
Respiratory rate 16
O2 saturation % 96
3
150,000–400,000
4500–11,000
Differential Diagnosis
Based on the patient’s initial symptoms upon arrival at the emergency department
[6], a wide range of reasonable differential diagnoses could’ve been formulated.
Listed below are the most important ones [6].
1. Myalgia– myalgia is a term used to describe muscle pain or discomfort. It is a
very common symptom associated with rhabdomyolysis, yet it can be absent in
many cases. Although myalgia is associated with rhabdomyolysis, it is only
diagnosed independently in uncomplicated cases to describe simple muscle pain
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M. J. Ghosheh
due to strain, overuse, or tension. In this case, the presentation of myalgia is due
to an underlying cause of rhabdomyolysis.
2. Infection – even though this patient’s temperature is high, the absence of an
elevated leukocyte count and localized symptoms such as redness and edema
makes this diagnosis unlikely. Moreover, this patient’s normal vital signs and
absence of hemodynamic instability rules out the possibility of a septic shock
due to a disseminated infection.
3. Inammatory myositis– this patient’s acute onset of symptoms without any pre-
vious complaints of muscle pain or weakness makes this diagnosis unlikely.
4. Congenital diseases (carnitine deciency, glycogen storage diseases) – this
patient’s onset and age of presentation with previous normal functionality and an
absence of similar family history makes this diagnosis unlikely.
Discussion
This patient’s nonspecic initial presentation of myalgia is unclear. Her diffuse
muscle pain is an alarming symptom signifying a more serious underlying condition. The extraordinary time spent at the gym with sudden-onset diffuse pain and
fever should’ve been further investigated. The early complications associated with
rhabdomyolysis are very important for a physician to be aware of. Electrolyte
abnormalities such as hyperkalemia, hyperphosphatemia, and hypocalcemia due to
their release from the myocytes can pose a serious threat to the patient [7]. Cardiac
arrhythmias and potentially cardiac arrest can be serious manifestations of electrolyte abnormalities. This patient’s electrolytes were tested for after readmission and
were abnormal. Late complications such as acute kidney injury due to the myoglobin released from the myocytes are a serious complication that presents with oliguria and darkening of the urine, as seen in this patient [7, 8]. These symptoms can be
reversed if the appropriate treatment was delivered in a timely fashion [9].
Understanding the pathophysiology behind rhabdomyolysis is very important.
The myocyte injury that occurs in rhabdomyolysis results in cell membrane injury
and hence the release of intracellular components, adenosine triphosphate phosphate (ATP) depletion, and generation of free radicals [10]. This results in the activation of cellular destructive processes through the activation of cellular proteases
and proteolytic enzymes. Ultimately, cellular destruction causes the release of
mainly potassium and myoglobin; both are largely the main triggers of arrhythmias
and acute kidney injury, respectively [11, 12].
The workup for patients with suspected rhabdomyolysis should mainly include,
complete blood count, serum chemistry (BUN, creatinine, uric acid, and liver function tests), lactate dehydrogenase, creatine kinase, and serum electrolytes (potassium, phosphate, calcium, and sodium) [9, 11]. The latest evidence-based approach
to treating patients with a conrmed diagnosis of rhabdomyolysis after targeting the
underlying cause is aggressive uid resuscitation and correction of the electrolytes
and acid-base abnormalities [10]. This essentially prevents end-organ complications
16 A Case ofMisdiagnosis ofRhabdomyolysis
109
that may develop. Electrocardiogram monitoring is also advised if the levels of
potassium get signicantly high. Alongside active management, monitoring the
patient for other complications like compartment syndrome, disseminated intravascular coagulation, and severe hypokalemia is very important. Finally, repeat creatinine kinase assays every 6–12 h are recommended to determine the peak creatinine
kinase levels [11, 12]. The incidence of rhabdomyolysis in the United States has
been reported to be as high as 26,000 cases annually, as of 2015 [7]. Considering the
relatively high number of misdiagnosed cases of rhabdomyolysis, a complete understanding of the presentation and potential complications is very important.
Conclusion
Rhabdomyolysis is a serious clinical syndrome that should be managed promptly. It
is commonly misdiagnosed in the emergency department due to its wide range of
nonspecic symptoms. A misdiagnosis would potentially put a patient at an
increased risk of developing severe and possibly fatal complications. Alarming
symptoms such as kidney injury, compartment syndrome, darkening of the urine,
and arrhythmias should be further investigated and managed. Rhabdomyolysis can
arise due to a wide range of causes; all can be classied under traumatic or nontraumatic causes. Traumatic causes of rhabdomyolysis and specically crush injuries
are the most common. In this case, this patient was misdiagnosed early on with
myalgia not related to rhabdomyolysis resulting in delayed treatment and consequently the development of serious complications of rhabdomyolysis. Therefore,
patients presenting with acute-onset diffuse muscle pain should be promptly tested
for creatinine kinase levels and electrolytes to rule out rhabdomyolysis.
References
1. Cabral B, Edding SN, Portocarrero JP, Lerma EV. Rhabdomyolysis. Dis Mon.
2020;66(8):101015. https://doi.org/10.1016/j.disamonth.2020.101015.
2. Zimmerman JL, Shen MC. Rhabdomyolysis. Chest. 2013;144(3):1058–65. https://doi.
org/10.1378/chest.12- 2016.
3. Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. New Engl J Med.
2009;361(1):62–72. https://doi.org/10.1056/NEJMra0801327.
4. Gupta A, Thorson P, Penmatsa KR, Gupta P. Rhabdomyolysis: revisited. Ulster Med
J. 2021;90(2):61–9.
5. King Faisal Specialist Hospital & Research Centre, 2022.
6. Khan FY.Rhabdomyolysis: a review of the literature. Neth J Med. 2009;67(9):272–83.
7. Baeza-Trinidad R. Rhabdomyolysis: a syndrome to be considered. Rabdomiólisis: un
síndrome a tener en cuenta. Med Clin. 2022;158(6):277–83. https://doi.org/10.1016/j.
medcli.2021.09.025.
8. Cordtz J.Rhabdomyolysis. Ugeskr Laeger. 2014;176(14):V11130695.
110
9. Long B, Koyfman A, Gottlieb M.An evidence-based narrative review of the emergency department evaluation and management of rhabdomyolysis. Am J Emerg Med. 2019;37(3):518–23.
https://doi.org/10.1016/j.ajem.2018.12.061.
10. Lee GX, Duong DK.Rhabdomyolysis: evidence-based management in the emergency department. Emerg Med Pract. 2020;22(12):1–20.
11. Bagley WH, Yang H, Shah KH.Rhabdomyolysis. Intern Emerg Med. 2007;2(3):210–8. https://
doi.org/10.1007/s11739- 007- 0060- 8.
12. Singh D, Chander V, Chopra K. Rhabdomyolysis. Methods Find Exp Clin Pharmacol.
2005;27(1):39–48. https://doi.org/10.1358/mf.2005.27.1.875435.
M. J. Ghosheh
Chapter 17
Acute Coronary Syndrome Misdiagnosed
asAnxiety
AlluriVasu
Learning Objectives
By the end of this presentation, the clinician will be able to:
1. Thoroughly evaluate patients presenting with pain anywhere in the region of
the chest.
2. Discuss the rationale of ordering serial ECG depending on the necessity to rule
out noncardiac from cardiac chest pain.
3. Rationalize additional investigations in patients with other comorbid conditions.
4. Discuss the justication of referring for expert care and management, for all
patients diagnosed with chest pain.
Introduction
Out of the several reasons for an emergency room (ER) visit, perhaps chest pain
happens to be among the top 5 [1]. On a given day, depending on how busy the day
was, doctors often nd it very difcult to come to a diagnosis of chest pain that
could be life-threatening vis-à-vis musculoskeletal. Pain in the region of the chest
can be as a result of several reasons and does not necessarily point toward cardiac in
origin. A casual review of medical literature will bring to light several instances
where chest pain was incorrectly assumed to be cardiac in origin leading to an
unpleasant situation for both the patient and the treating doctors often ending in
A. Vasu (*)
St. Martinus University Faculty of Medicine, Willemstad, Curacao
e-mail: alluri.vasu@martinus.edu
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
H. Tohid et al. (eds.), The Misdiagnosis Casebook in Clinical Medicine,
https://doi.org/10.1007/978-3-031-28296-6_17
111
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A. Vasu
lawsuits. More often than not, the symptoms associated with diseases of the gastrointestinal tract present with symptoms in the region of the chest which the patients
assume to be pain that actually might have been heartburn, a common symptom of
reux esophagitis. Musculoskeletal pain in the region of the chest following a blunt
injury to the chest or a fall is one of the several reasons for patients seeking medical
attention. Women and patients who are anxious are a challenging group of patients
who often present with ambiguous symptoms and require additional efforts from
the treating physician to come to a reasonable diagnosis in the ER setup. If the rst
point of contact is a weak link in the chain of events, there is every possible reason
for that patient ending up treated inappropriately. In that particular group of patients
like smokers, diabetics, and the elderly, the symptoms and signs of many diseases
are masked or overlapped, and it becomes particularly challenging to come to an
appropriate diagnosis in the ER given the paucity of time. It is the responsibility of
the senior doctors to train the new doctors in the nuances of the art of medical practice to come to a reasonable diagnosis in the shortest time possible, and it goes a
long way in establishing condence in the doctors undergoing training. Medical
practice does not permit any room for misdiagnosis, and mistakes that occur unintentionally often end up as tragedy for all those involved. Misdiagnosis of chest pain
and the associated implication for that patient can be life-changing [2]. Many a time
doctors take the help of additional diagnostic tools to differentiate between relevant
and irrelevant [3] chest pain. It is always a good practice to take a second look or
seek additional help from a senior colleague when in doubt about the diagnosis, and
that goes a long way in helping both the patients and as well as the medical fraternity. Chest pain should get the evaluation it deserves as any lapse can be lifechanging, regardless of its origin, and it should always be evaluated by a medical
doctor. Many times, most patients with chest pain are treated in the ER without the
need for additional tests or physician visits. The only problem is in deciding if chest
pain can wait till the next physician appointment. The patients should not take
chances and make it possible, to at least, visit a medical doctor who can further
advise them on treatment and diagnosis. There have been several groundbreaking
diagnostic tests to diagnose chest pain of cardiac origin, but their use is based on the
suspicion of cardiac chest pain at presentation. The diagnosis or misdiagnosis of
chest pain in the ER is largely dependent on the presence of trained staff who can
differentiate cardiac from noncardiac chest pain. Today, many point-of-care devices
as well as elevated levels of enzymes are being used to diagnose cardiac chest pain
within the “golden hour,” as suggested by recent data from several large clinical trials; treatment done within that golden hour salvages the myocardium to a large
extent. Statistically, most misdiagnosis occurs in those patients presenting to ER
either late into the night or while changing shifts. The reasons are obvious. Many
hospitals have brought about standard operating protocols to overcome these difculties and minimize misdiagnosis. But despite the many advances in medical sciences, chest pain happens to be a frequently misdiagnosed medical emergency. We
17 Acute Coronary Syndrome Misdiagnosed asAnxiety
113
bring forward one such case which was almost misdiagnosed as noncardiac
chest pain.
Clinical Case Presentation
A 40-year-old, obese male presented to the ER with a brief history of ongoing
chest pain of 1 h duration. The patient was recently diagnosed with diabetes and
was struggling to give up smoking. He had on arrival at the ER confessed about
the binge drinking party during the long weekend and having to enjoy a wide
variety of food. The patient denied any injury or trauma to the chest. The patient
was evaluated by the ER physician who after a careful history and examination
concluded that the patient was having acid reux disease as the chest pain was
atypical; however, more for the sake of completion, he advised an ECG for the
patient, who with great reluctance complied with the request. ECG was done and
reported to be normal. He was reassured and advised proton pump inhibitors for
6weeks, and an appointment with his family physician was xed. The patient,
although not fully relieved of the pain, nonetheless decided to go with the doctor’s
advice. But an hour later, he presented again with worsening pain and cold
clammy extremities. This time he was seen by a different ER physician, who after
spending a brief time with the patient and quick history was convinced that he was
dealing with a psychiatric patient who was having atypical chest pain, nothing
more than a gastric esophageal disease, and was desperate to seek medical attention. This time he was administered some intravenous painkillers and advised to
return if there wasn’t any relief of symptoms. This patient visited the ER a third
time with ongoing chest pain of 5 h duration and was unconscious at presentation.
He was seen by a third ER physician and after taking the history from the attenders
and the fact that this was his third visit to ER with chest pain. He was admitted to
the hospital. A brief workup showed a blood pressure of 80/60mmHg, random
blood glucose of 160mg/dL, and rapid low volume pulse. Intravenous access was
established, uids were started, and a repeat ECG was advised. ECG was shared
with a consultant who was quick to diagnose an ongoing acute inferior-posterior
ST elevation myocardial infarction. Under the supervision of a cardiologist, the
patient was admitted to the intensive care unit who shifted the patient to the cardiac catheterization lab; a quick coronary angiogram demonstrated 100% occlusion of the left circumex artery. Patient attendees were explained the need for
further intervention, and the left circumex artery was opened. Following the
treatment, the patient regained consciousness, blood pressure normalized, and
chest pain had decreased considerably. The patient was moved to the intensive
care unit where he was observed for further 24h and after 3 days was discharged
from the hospital. He made a good recovery and will follow up with his family
physician.