Community EM

Cases from the Community: Springing a Leak

Case

A 58 year-old male, with history of kidney stones and appendectomy, presents to the ED with complaint of left lower quadrant abdominal pain. The patient goes on to describe waxing and waning “deep” and moderately severe pain in the abdomen with radiation to the back for two days. He notes associated nausea and one episode of dark urine but denies any fevers, nausea, vomiting, diarrhea, or any other urinary symptoms. He reports the pain is similar to prior episode of kidney stones, but feels more anterior.

Vital Signs

BP 177/93 | Pulse 87  | Temp 98.1 °F (36.7 °C)  | Resp 20  | SpO2 97%

Exam
Constitutional: Well-developed, in no apparent distress.

Cardiovascular: Normal rate and regular rhythm.  

Pulmonary/Chest: Effort normal and breath sounds normal. He has no wheezes. He has no rales.

Abdominal: Soft. Focal left local quadrant tenderness, No rebound, rigidity or guarding.  

GU: Normal testicular lie, no tenderness or erythema of the testicles. Normal cremasteric reflex. No costovertebral angle  tenderness.

Workup

Labs performed including complete blood count and basic metabolic profile are within normal limits, with a creatinine of 0.74. Urinalysis demonstrates 10 red blood cells, 1 white bell cells, and is otherwise within normal limits.

Given the patient’s significant abdominal pain, Computed tomography (CT) abdomen/pelvis with contrast is performed:

Image 1.png
Figure 1: Axial and coronal views of the CT abdomen/pelvis.

Figure 1: Axial and coronal views of the CT abdomen/pelvis.

Diagnosis

Spontaneous calyceal rupture

Radiologic impression

Mild left hydronephrosis, with moderate to severe perinephric and lower left retroperitoneal fluid concerning for recent calyceal rupture. No discrete obstructing calculus currently visualized. Of note, there is a 1.1 cm calculus in the left renal pelvis. In addition, given, extensive fluid, superimposed infection cannot be excluded.

Discussion

The above case is a classic example of a not-too-common urologic finding in the ED: spontaneous calyceal rupture. This finding is thought to occur as a result of a sudden increase in pressure in the collecting system. Most commonly, this sudden increase pressure is due to an obstructing kidney stone (typically in the distal ureter), however, it has also been described in the setting of other pathologies that obstruct the urinary system, including cancer, prostatic hypertrophy, pregnancy, and abdominal aortic aneurysm, as well as iatrogenic causes. The collecting system, typically a low-pressure system, is poorly equipped to handle the sudden increase in pressure, and ruptures in the most susceptible part of the system — the calyx. More specifically, it is the fornix, the lateral aspect of the minor calyx, that is the most common culprit (Figure 1).

Figure 2: Anatomy of the kidney.

Figure 2: Anatomy of the kidney.

Most cases of calyceal rupture present with flank pain, nausea, and vomiting, although more severe symptoms, such as severe abdominal pain and systemic findings, can occur. Rupture results in extravasation of urine that can collect around kidney or even in the retroperitoneum. The feared complication of this process is infection of the urine collection, leading to perinephric abscess formation and sepsis. The diagnosis is made either via ultrasound or CT.

Management first involves relieving the cause of obstruction. In the ED, if the obstruction is secondary to prostatic hypertrophy a foley should be placed. The patient should receive hydration and analgesia. Urology should be consulted to understand which patients will need intervention such as stenting or lithotripsy. At this time there is no standard as to the appropriateness of antibiotic therapy. Of course, if a patient shows evidence of infection, antibiotics (and source control) are indicated. However, if a patient demonstrates no systemic signs of infection and has a negative urinalysis it is reasonable to consider deferring antibiotics at the index visit. This decision, as well as whether to admit or discharge the patient should be made in conjunction with our urology colleagues.

Case conclusion

The patient was managed conservatively with fluids and analgesia. Antibiotics were deferred in consultation with Urology. The patient was discharged to close urologic follow-up. At four month chart review the patient had suffered no further complications and no long term sequelae from his calyceal rupture.  

 Faculty Reviewer: Dr. Kristy McAteer


References

  1. Al-Mujalhem AG, Aziz MS, Sultan MF, Al-Maghraby AM, Al-Shazly MA. Spontaneous forniceal rupture: Can it be treated conservatively? Urol Ann 2017:9(1);41-44 

  2. Doehn C, et al. Outcome analysis of fornix ruptures in 162 consecutive patients. J Endourol 2010;24(11):1869-73.

  3. Morgan TN, Bandari J, Shahait M, Averch T. Renal forniceal rupture: Is conservative management safe? Urology 2017;109:51-54.

  4. Tanwar S, Joshi A. A blow-out. Am J of Med 2011;124(1):37-39.

  5. https://opentextbc.ca/anatomyandphysiology/chapter/25-3-gross-anatomy-of-the-kidney/

Fibrinolytic Therapy for STEMI

Case

You are on a swing shift at a remote, island-based community hospital when a 58 year-old male presents with sudden onset chest pain. The pain started at rest, radiates to his jaw, and is associated with diaphoresis and nausea. He has a history of coronary artery disease (CAD), and during his last cardiac catheterization in 2008, a stent was placed in his proximal left anterior descending coronary artery. His past medical history is also significant for diabetes, chronic obstructive pulmonary disease, hyperlipidemia, and hypertension.  He is an active smoker.

On exam, he is not only diaphoretic and clenching his chest, but also describes the pain as “an elephant sitting on my chest.” Initial vital signs are P 110, BP 175/100, RR 20, PO2 98% on RA, T 98.9 F. You give him aspirin 324 mg and nitroglycerin sublingual 0.4 mg, and his chest pain improves from a 10/10 to 8/10. His initial electrocardiogram (EKG) is below.

Figure 1: The patient’s presenting EKG.

Figure 1: The patient’s presenting EKG.

DIAGNOSIS

ST elevation myocardial infarction (STEMI)

Management Options

You call the critical care transport ambulance, as well as the nearest cardiac catheterization team to alert them of your patient.   Unfortunately, it is a stormy evening in the middle of winter and all bridges off the island are closed; helicopters are grounded due to the storm.  There are no transfer options available to your patient at this time. What else can you do?

Indications for Fibrinolytic Therapy

According to the American Heart Association, there are several considerations when it comes to fibrinolytic therapy in myocardial infarction:

Class I recommendations:

  1. STEMI

  2. Symptom onset in the last 12 hours

  3. Percutaneous Cardiac Intervention (PCI) cannot be performed within 120 minutes of arrival to the Emergency Department

  4. Absence of any contraindications (see below)

Class II recommendations:

  1. Evidence of ongoing ischemia 12-24 hours after symptom onset

  2. Large area of myocardium affected

  3. Hemodynamic instability

Absolute contraindications:

  1. Any prior intracranial hemorrhage

  2. Known structural cerebral vascular lesion

  3. Ischemic stroke <3 months

  4. Suspected aortic dissection

  5. Known intracranial malignancy

  6. Active bleeding or bleeding diathesis

  7. Significant closed head trauma <3 months

  8. Intracranial/intraspinal surgery <2 months

  9. Severe uncontrolled HTN (>175/110)

  10. Oral anticoagulants

Relative contraindications:

  1. Significant HTN on arrival (pressure > 180 mmHg)

  2. Ischemic stroke >3 months

  3. Dementia

  4. Other intracranial pathology

  5. Traumatic CPR >10 min

  6. Major surgery <3 weeks

  7. Internal bleeding <3 weeks

  8. Non-compressible vascular punctures

  9. Pregnancy

  10. Active peptic ulcer disease

PCI versus Systemic Fibrinolytic Therapy

If you are able to transfer the patient to a hospital with PCI capability within 1 hour of presentation or they have contraindications to fibrinolytic therapy, it is recommended that you transfer the patient as soon as possible. Otherwise, the goal is fibrinolytic infusion within 30 minutes of arrival to the ER. In either case, concurrently initiate maximal medical management including full-dose aspirin, Plavix or Brilinta, and anticoagulation (unfractionated heparin or lovenox). Tenecteplase is generally the preferred fibrin-specific agent, given its ease of use and lower rates of non-cerebral bleeding compared to other agents.

Reassess After Fibrinolysis

If your patient has resolution of chest pain and >70% reduction of ST elevation, or ST elevation resolves within 60-90 minutes, you have likely restored flow. If you see <50% decrease in STE and no reperfusion arrhythmias (see below) at 2 hours after fibrinolytic dosing, you have partially improved flow but not completely restored it.

Criteria for Transfer after fibrinolytic therapy

  1. Immediate transfer: acute heart failure or cardiogenic shock

  2. Urgent transfer: failed reperfusion or reocclusion

  3. 3-24 hours: hemodynamically stable, successful reperfusion

Reperfusion Arrhythmias 

You plan for ICU admission because you are unable to transfer the patient to a PCI center when the nurse hands you the following EKG:

Figure 2: Accelerated idioventricular rhythm.

Figure 2: Accelerated idioventricular rhythm.

This is an example of accelerated idioventricular rhythm. This is a normal sign of reperfusion after STEMI and does not require treatment.   In fact, such a rhythm is generally viewed as a positive response to fibrinolytic therapy as indicates reperfusion. 

Criteria:

  1. Regular rhythm

  2. Rate 50-110bpm (slower is ventricular escape, faster is VT)

  3. Three or more ventricular complexes

  4. Fusion (F) and capture (C) beats (see below)

Figure 3: Fusion and capture beats after successful reperfusion.

Figure 3: Fusion and capture beats after successful reperfusion.

General goals of care after fibrinolytic therapy should be to transfer for diagnostic angiography and percutaneous coronary evaluation which is promptly accomplished for your patient the following day after the storm resolves.


Faculty reviewer: Dr. Kristina McAteer


References

  1. O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013; 127:529.

  2. O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013; 127:e362.

  3. White HD. Thrombolytic therapy in the elderly. Lancet 2000; 356:2028.

  4. Armstrong PW, Gershlick AH, Goldstein P, et al. Fibrinolysis or primary PCI in ST-segment elevation myocardial infarction. N Engl J Med 2013; 368:1379.

  5. Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI). Lancet 1986; 1:397.

  6. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Lancet 1988; 2:349.
    Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Fibrinolytic Therapy Trialists' (FTT) Collaborative Group. Lancet 1994; 343:311.

  7. Labinaz M, Sketch MH Jr, Ellis SG, et al. Outcome of acute ST-segment elevation myocardial infarction in patients with prior coronary artery bypass surgery receiving thrombolytic therapy. Am Heart J 2001; 141:469.

  8. Peterson LR, Chandra NC, French WJ, et al. Reperfusion therapy in patients with acute myocardial infarction and prior coronary artery bypass graft surgery (National Registry of Myocardial Infarction-2). Am J Cardiol 1999; 84:1287.

  9. Karnash SL, Granger CB, White HD, et al. Treating menstruating women with thrombolytic therapy: insights from the global utilization of streptokinase and tissue plasminogen activator for occluded coronary arteries (GUSTO-I) trial. J Am Coll Cardiol 1995; 26:1651.

  10. Woodfield SL, Lundergan CF, Reiner JS, et al. Angiographic findings and outcome in diabetic patients treated with thrombolytic therapy for acute myocardial infarction: the GUSTO-I experience. J Am Coll Cardiol 1996; 28:1661.

  11. Mak KH, Moliterno DJ, Granger CB, et al. Influence of diabetes mellitus on clinical outcome in the thrombolytic era of acute myocardial infarction. GUSTO-I Investigators. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries. J Am Coll Cardiol 1997; 30:171.

Meeting Uncle Rhabdo

rhabdo.png

THE PATIENT:

A 28 year old previously healthy male presents to the emergency department with concerns for worsening back pain that is predominantly left sided and along the lumbar spine. Two days prior to the visit he recalls a work out that consisted of many dead lifts. He also played basketball the following day and rode his bike into work, which is more activity than usual for him. He tried NSAIDs for pain control, but his pain is more intense and he noticed his urine looked brown today. He denies any fevers, history of IVDU, weight gain or loss, urinary tract infections or STDs, immunosuppression, recent spinal fracture or procedure, incontinence or retention.

PHYSICAL EXAMINATION:

144/83, 82, 37.1, 18, 98%

Gen: well appearing, no acute distress

HENT: normocephalic, MMM

CV: RRR

Pulm: CTAB

Abd: soft, nontender, nondistended

MSK: muscle spasms along the left lumbar paraspinal muscle, no midline tenderness to palpation, muscle compartments in the upper and lower extremities are soft

Neuro: L1-S5 strength 5/5 and sensation to light touch is intact

Skin: pink, warm, dry

THE COURSE:

As an experienced clinician you are able to quickly arrive at a diagnosis of rhabdomyolysis from the brief history and physical exam, but what else needs to be done? In the emergency department we need to initiate diagnostic studies to evaluate the severity of illness and help plan for an appropriate disposition. Thankfully, your history and exam reveal no red flag findings for more concerning etiologies of back pain, so your evaluation can be quite focused. The patient had lab work sent off and was provided with IVF boluses and given analgesia with marked improvement in his symptoms. He was admitted to the medical floor for continued care for the next couple days.

THE WORK UP:

CK >20,000 IU/L (labs upper limit for reporting without further analysis and quantitative estimates, normal range 20-210, remained >20,000 for 5 consecutive days) finally on day 6 CK 10, 933 IU/L

BMP: Glu 113, BUN 19, Cr 1.0 (on discharge was 0.84), Na 139, K 3.8, Cl 104, CO2 29, Ca 8.9

Urinalysis: Brown, cloudy, trace ketones, specific gravity >1.03, blood 3+, protein >300

Urine microscopic analysis: RBC none seen, WBC 3, amorphous crystals present

Urine myoglobin: >8,750 mcg/ml (normal range < 28mcg/ml)

DISCUSSION:

The key clinical manifestations of rhabdomyolysis include a triad of muscle tenderness and weakness as well as dark urine, so the triage note already had it set up on a silver platter for you. Remember, however, as with any triad in medicine this classic presentation is rare. Some studies revealed that over half of patients do not report muscle pain or weakness. Rhabdomyolysis occurs due to muscle necrosis and the release of intracellular contents into the circulation. Patients may present with a wide range of symptoms and the most concerning complications include hyperkalemia, renal failure and rarely disseminated intravascular coagulation. Patients who present with concomitant acute kidney injury tend to have worse outcomes and the mechanism of injury is primarily related to the nephrotoxic effects of myoglobin. In an acidic environment myoglobin may precipitate and subsequently damage the kidneys by obstruction of the renal tubules, cause oxidative damage and vasoconstriction.

The etiologies of rhabdomyolysis can be broken up into four broad categories: impaired production or use of ATP, dysfunctional oxygen or nutrient delivery, increased metabolic demand exceeding capacity, and direct myocyte damage. Recently, on EM: RAP Dr. DeLaney argued that this can be further simplified into two broad categories, exertional and non-exertional. Classic cases include trauma patients who have crush injuries but can also occur with heat related illnesses such as heat exhaustion or stroke, or in cases of hyper-kinetic states. Medications implicated in this disease process include antipsychotics and statins as well as others such as illegal drugs like cocaine.

CK levels classically rise within two to twelve hours after the onset of injury and peak within three days. The level should return to baseline within ten days. The diagnosis is often considered if the CK level is above five times the upper limit of normal at presentation, roughly 1,000 IU/L. More discrete categories can also be used to differentiate mild to severe cases based on CK levels, however, it is the degree of renal impairment that likely has the greatest role on patient outcome. Emergency department management includes aggressive IVF hydration with a target urine output of approximately 250 ml/hr and attempts to identify and correct the underlying pathology. Some argue for urinary alkalinization; however, the literature is limited with regards to strong recommendations on this topic. Common electrolyte abnormalities include: hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia. Disseminated intravascular coagulation can rarely be seen as a result of thromboplastin and prothrombotic agents released from damaged myocytes. Acute kidney injury is more common if the presentation includes a CK >5,000 IU/L and in cases with sepsis, acidosis, or dehydration. Ultimately, most patients do well during their hospital courses and rarely require significant interventions, but mortality may be upwards of 20% in those that present with significant kidney injury noted at the time of presentation, therefore, careful evaluation of the patient’s lab studies and admission for close observation remains the mainstay of treatment.

Faculty Reviewer: Dr. Gita Pensa

SOURCES:

  1. DeLaney, M. “Rhabdomyolysis: Part 1 Diagnosis and Treatment.” www.emrap.org March 2018, 18 (3)

  2. DeLaney, M. “Rhabdomyolysis: Part 2 Disposition.” www.emrap.org March 2018, 18 (3)

  3. Majoewsky, M. “Rhabdomyolysis: C3 Project.” www.emrap.org June 2012, 2 (6)

  4. Sauncy, H. (2017). Don’t Get Broken Up About Muscle Breakdown. In Mattu, A. Marcucci, L. et al (Eds.), Avoiding Common Errors in the Emergency Department: Second Edition (pp. 414-16). Philadelphia: Wolters Kluwer.