SPIN

PGI SIBAYAN, QUENNA LIZA T.

CSMC GROUP 6
IDENTIFYING
DATA
K.C.
35/M Single
from Antipolo, Rizal
works as a flight attendant
TEA COLORED URINE
1 day duration
CHIEF COMPLAINT
HISTORY OF PRESENT ILLNESS
3 days 1 day
PTA PTA Day of
Interim
Admission
Tea-colored
Spinning urine
Persistence of
class symptoms
“C2-like” Persistence of
symptoms
Lower No change in
extremity Partially volume/frequency, dysuria, ER consult
muscle pain relieved with flank pain, fever, cough,
colds, nausea/vomiting,
intake of jaundice, abdominal pain, Advised
Ibuprofen and or change in diet admission
Naproxen
 PAST MEDICAL HISTORY

NO PREVIOUS
NO KNOWN NO KNOWN
COVID-19
COMORBIDS ALLERGY
INFECTION
No previous Food or medication
hospitalization Fully vaccinated
or surgery Primary: Sinovac
Booster: Moderna x 1 dose
(May 2022)
 FAMILY SOCIAL
HISTORY HISTORY

HYPERTENSION NONSMOKER
Both parents
OCCASIONAL
ALCOHOLIC
BEVERAGE DRINKER
 PHYSICAL EXAM
INITIAL VS 130/90mmHg > 90bpm > 19cpm > 36.6C > 98% at room air

Awake, alert, ambulatory, comfortable, not in cardiorespiratory distress

GENERAL SURVEY Ht 173cm Wt 77.3kg BMI 25.8kg/m2 (Obese I)

HEENT Anicteric sclerae, pink palpebral conjunctiva, moist oral mucosa

CHEST/LUNGS No deformities, symmetrical chest expansion, clear breath sounds

CARDIOVASCULAR Normal rate, regular rhythm, no murmurs

ABDOMEN Flat, normoactive bowel sounds, soft, nontender, no CVA tenderness

Full and equal pulses, CRT<2s, bilateral thigh tenderness,

EXTREMITIES proximal weakness 4/5 distal 5/5, no edema
 SALIENT FEATURES

HISTORY OF MUSCLE PAIN

STRENUOUS ON LOWER
EXERCISE EXTREMITIES

TEA-COLORED BILATERAL
URINE THIGH
TENDERNESS
RHABDOMYOLYSIS
PRIMARY IMPRESSION

Classic triad: myalgia, red to brown urine,

elevated serum muscle enzymes

History of extreme physical exertion

 DIFFERENTIAL DIAGNOSES
RENAL
✓ tea-colored urine
URINARY TRACT ✗ fever/chills, dysuria, frequency, urgency,
INFECTION hypogastric/flank pain, nausea/vomiting, CVA
tenderness

✓ tea-colored urine
NEPHROLITHIASIS ✗ flank pain, dysuria, urgency, nausea/vomiting, CVA
tenderness

✓ tea-colored urine
POST-STREPTOCOCCAL
✗ no recent URTI or skin infection, fever,
GLOMERULONEPHRITIS cough/colds, hypertension, edema
 DIFFERENTIAL DIAGNOSES
GI
✓ tea-colored urine
HEPATITIS ✗ fever, nausea/vomiting, jaundice, abdominal pain,
clay-colored stools

✓ tea-colored urine
CHOLEDOCHOLITHIASIS ✗ RUQ/epigastric pain, nausea/vomiting, clay-colored
stools, jaundice, RUQ/epigastric tenderness

OTHERS
✓ NSAIDs (ibuprofen, naproxen)
MEDICATION-INDUCED
✗ nitrofurantoin, metronidazole, chloroquine,
TEA-COLORED URINE
primaquine
DIAGNOSTICS
Total CK (CK-MM, CK-MB)
Urinalysis

CBC
Crea, BUN, Uric acid
Na, K, Ca, Phosphorus

SGPT, SGOT
LABORATORY RESULTS
LABORATORY RESULTS
LABORATORY RESULTS
 MANAGEMENT
Volume
administration
Insert IV access
Hydrate with PNSS
initially to run at 1-2L/hr
then titrate according to
volume status and urine
output (200-300mL/hr)
Urinary
alkalinization
Sodium Bicarbonate 150meqs
in 1L D5W to run at 200mL/hr
or 650mg/tab 1 tab 3x/day
Monitoring
Crea, Urinalysis
Total CK (CKMM, CKMB)
CASE
DISCUSSION
RHABDOMYOLYSIS
ETIOLOGY
● Traumatic or muscle compression
○ Crush syndrome
○ Prolonged immobilization
● Nontraumatic exertional
○ Marked exertion in untrained individuals
○ Eccentric exercises
○ Hyperthermia
● Nontraumatic non-exertional
○ Drugs (statins) or toxins
○ Infections
○ Electrolyte disorders
 PATHOPHYSIOLOGY
● Direct myocyte injury or ATP depletion →
dysfunction of Na+/K+ ATPase and Ca2+
ATPase pumps (myocyte integrity) →
myocyte injury → release of intracellular
muscle components (CK, myoglobin (heme),
various electrolytes) → increase in
intracellular Ca2+ → activation of proteases,
increased skeletal muscle contractility,
mitochondrial dysfunction, production of
ROS → skeletal muscle cell death
 CLINICAL MANIFESTATION
Nausea/ vomiting
Abdominal pain Malaise, fever,
tachycardia

Muscle pain,
stiffness/cramping
Dark urine
Proximal muscle groups -
thighs, calves,
shoulders, lower back
COMPLICATIONS
● Fluid and electrolyte abnormalities
○ Hypovolemia
○ Hyperkalemia,hyperphosphatemia,
hypocalcemia, hyperuricemia
○ Metabolic acidosis
● Acute kidney injury
● Compartment syndrome
 REFERENCES

● Torres, P. A., Helmstetter, J. A., Kaye, A. M., & Kaye, A. D. (2015).

Rhabdomyolysis: Pathogenesis, diagnosis, and treatment. The Ochsner
journal. Retrieved October 28, 2022, from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4365849/
● Bhai, S., & Dimachkie, M. M. (2022). Causes of rhabdomyolysis, Clinical
manifestations and diagnosis of rhabdomyolysis. UpToDate. Retrieved
October 28, 2022, from https://www.uptodate.com
● Perazella, M. A., & Rosner, M. H. (2022). Prevention and treatment of
heme pigment-induced acute kidney injury (including rhabdomyolysis).
UpToDate. Retrieved October 28, 2022, from https://www.uptodate.com
THANKS!
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