Can’t Miss Surgical Emergencies – Part 2

Authors: Sarah Brubaker, MD (EM Resident at SAUSHEC, US Army) and Brit Long, MD (@long_brit, EM Attending Physician at SAUSHEC) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW Medical Center / Parkland Memorial Hospital)

This is the second in a two-part series discussing can’t-miss diagnoses that may require emergent surgical intervention. Part 1 ( included ruptured ectopic pregnancy, ruptured AAA, and aortic dissection. In this article, we will explore three more disease processes that can be easy to miss, though delay in diagnosis and treatment can lead to long-term sequelae and even death. So, without further ado, let’s jump right in to discuss three more surgical emergencies.

Case 1:

A 63-year-old male with a history of insulin-dependent diabetes, CHF, and stage II CKD presents with a painful “rash” on his left thigh. He noticed it for the first time this morning. On exam, he is slightly tachycardic, normotensive, and has a fever of 101.0 ͒F. He has an area of warm, mildly tender erythema in the inner left thigh.


Epidemiology and Risk Factors

Necrotizing soft tissue infection is a rare but deadly clinical entity. According to a large cohort study in Texas, the incidence of necrotizing fasciitis has increased in the past decade (1), perhaps due to increased clinical suspicion and awareness. In this study, 72% of patients had one or more comorbidities, and the most prevalent risk factor was diabetes (48%), followed by obesity (15%). Another study found that patients with diabetes and obesity are also more likely to die as a result of necrotizing infection (2). Other risk factors include chronic alcoholism, peripheral vascular disease, heart disease, renal failure, decubitus ulcers, chronic skin infections, intravenous drug abuse, and immunocompromised states such as HIV or cancer (3,4). However, necrotizing fasciitis can also present in young, healthy individuals!

Even with prompt diagnosis and optimal treatment, necrotizing fasciitis portends high morbidity and mortality (5).  Mortality rates are classically described as 25-35%, but they have been steadily decreasing, and mortality is currently estimated to be approximately 10% in the United States (1,4).  Despite declining mortality rates, more patients are discharged to long-term facilities with debilitating conditions (1).


Most necrotizing infections are secondary infections–they develop from an initial break in the skin, usually related to accidental or iatrogenic trauma (3). According to IDSA guidelines, 80% of necrotizing skin infections result from the extension of an initial, often minor, skin lesion. These small lesions, caused from external trauma such as IV injection, surgical incision, abscess, insect bite, or decubitus ulcer, lead to direct invasion of the subcutaneous tissue that results in a rapidly spreading necrotizing process (1). The remaining 20% have no visible skin lesion, and while spontaneous development of necrotizing fasciitis is rare, patients with diabetes and malignancy are at increased risk (3).

Spread of infection below the subcutaneous tissue leads to thrombosis of the capillary beds under the skin. However, a large number of capillary beds must thrombose before dermal involvement becomes apparent, so physical exam findings do not accurately represent the extent of necrotizing infection. An ischemic tissue environment promotes bacterial growth, propagating the process and resulting in rapid spread of infection. Thus, infection can spread as quickly as one inch per hour (4)! As the disease progresses, widespread gangrene of the skin, subcutaneous tissue, fascia, and even skeletal muscle may occur. These are late findings that portend poor prognosis, so it is important to diagnose necrotizing infection long before these findings become apparent.

Necrotizing skin infections can be categorized into three groups: polymicrobial (type I), monomicrobial due to Strep or Staph species (type II), and infection due to Vibrio vulnificus (which some refer to as type III), more common in cirrhotics) . Polymicrobial infections are more common than monomicrobial. They occur after surgery or in patients with peripheral vascular disease, diabetes, decubitus ulcers, or mucosal tears of GI/GU tract (i.e. Fournier’s gangrene). Cases of necrotizing fasciitis that arise after varicella infection or after trivial injuries like minor scratches/insect bites are almost always monomicrobial, caused by Strep pyogenes. The mortality in this group is high, approaching 50-70% in patients with hypotension and organ failure (3).

Clinical presentation

The classic presentation of necrotizing fasciitis is a patient with severe pain, anxiety, and diaphoresis, sometimes with systemic symptoms such as fever and nausea (3). However, the clinical presentation for patients with necrotizing fasciitis is very non-specific. Patients may present with only a small area of cellulitis, which can rapidly spread in a short amount of time. Patients often describe excruciating pain at the site of infection. Only 10-45% of patients report trauma or a break in the skin prior to onset of symptoms (3). The most important historical clue is the rate of spread of infection. Therefore, it is important to inquire about how quickly the symptoms have progressed, how quickly the cellulitis has spread, and whether the patient has already been diagnosed with cellulitis but has failed antibiotic management.

Physical exam

Because necrotizing fasciitis spreads so quickly, it can initially be difficult to distinguish between cellulitis and necrotizing infection. Patients often present with abnormal vital signs, such as tachycardia and fever, in addition to disorientation or lethargy. Exam features that suggest deep infection include severe, constant pain, bullae (related to occlusion of deep blood vessels that traverse the fascia or muscle compartments), skin necrosis or ecchymosis that precede skin necrosis, gas in the soft tissues (detected by palpation or imaging), edema that extends beyond the margin of erythema, cutaneous anesthesia, systemic toxicity (manifested by fever, leukocytosis, delirium, and renal failure), and rapid spread, especially despite antibiotic therapy (6).

The classic description of necrotizing fasciitis is excruciating pain associated with only a small area of cellulitis, with tenderness beyond the area of erythema. Thus, the catch-phrase for necrotizing fasciitis is “pain out of proportion to exam findings.” However, as the condition develops, the affected areas may become insensate. It is important to evaluate for the presence of subcutaneous emphysema at the site of infection. When anesthesia, bullae, skin sloughing, rapid progression, or crepitus are present, emergent surgical evaluation is necessary (1,3,6). However, the only signs present in more than half of patients with necrotizing fasciitis are erythema, tenderness, and marked edema beyond the area of redness. Crepitus occurs in only 13-31% of patients (3).


The Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score is the most popular tool used to risk-stratify patients with suspected necrotizing fasciitis. Points are assigned based on lab values: CRP, WBC, hemoglobin, serum creatinine, and glucose. A score greater than six indicates high risk for necrotizing fasciitis. The initial study reported a positive predictive value of 94% and a negative predictive value of 96% in patients with scores higher >6 (7). Patients with a score higher than six also have a higher rate of mortality and amputation (8). However, despite its widespread use, the LRINEC score has never been validated, and it was originally retrospectively derived. In addition, several studies have questioned its sensitivity (which, at best, is 80%) (9,10,11) and its specificity (65% in the initial study) (7).

Infectious Diseases Society of America (IDSA) guidelines recommend the following tests for evaluation of a patient with suspected necrotizing fasciitis: blood cultures with drug susceptibility testing, CBC with differential, creatinine, bicarbonate, creatine phosphokinase, and CRP (12). Hospitalization should be considered in patients with hypotension, elevated creatinine, low sodium bicarbonate, elevated creatine phosphokinase (2-3 times the upper limit of normal), marked WBC left shift, or CRP greater than 13 mg/L. These patients also warrant aggressive diagnostic measures, usually surgical exploration.

It is important to note that necrotizing fasciitis is a clinical diagnosis. Laboratory values are nonspecific and minimally helpful in making the diagnosis. The most helpful finding on Xray is subcutaneous emphysema, but this only found in up to 25% of cases of confirmed necrotizing fasciitis (13). In addition, CT and MRI also have poor sensitivity in identifying and characterizing necrotizing soft tissue infection (12). Necrotizing fasciitis may not present with any abnormalities on CT imaging, but it may be visible as edema extending along the fascial plane, with or without emphysema. Obtaining advanced imaging is often unhelpful, and it may delay appropriate treatment and referral to a surgeon.

Ultrasound is emerging as a potential diagnostic modality. Several case studies have detailed incidences in which ultrasound was able to identify and characterize necrotizing infections missed by CT but subsequently confirmed in the OR (14).

Surgery is the most important diagnostic and therapeutic modality! Necrotizing fasciitis spreads incredibly rapidly, so prompt treatment should not be delayed by obtaining labs and imaging. If there is a high suspicion for necrotizing fasciitis, but the diagnosis cannot be confirmed, the patient should be brought to the operating room for an exploratory incision with the potential for further debridement.


Early diagnosis and intervention are essential because mortality is directly associated with time to initial intervention (15). Even with optimal treatment, necrotizing soft tissue infections portend significant morbidity and have mortality rates of 25-35%.  If a patient presents with a history and physical exam concerning for necrotizing fasciitis, initiate antibiotic therapy immediately. Because necrotizing infections are often polymicrobial, broad-spectrum coverage is necessary; the preferred antibiotics are vancomycin or linezolid plus piperacillin-tazobactam or a carbapenem; or ceftriaxone plus metronidazole (12). Clindamycin should be added due to its effects on toxin inhibition. If concern for Vibrio is present, doxycycline is required. However, the tissue ischemia associated with deep infection prevents adequate delivery of oxygen and antibiotics to the damaged tissue. Thus, antibiotics alone are not an effective treatment, and emergent surgical consult is necessary.

Case 2:

A 13-year-old boy presents with severe, vague abdominal pain that woke him from his sleep approximately 1 hour ago. He feels slightly nauseated and has vomited once. His vitals and physical exam are within normal limits.


Epidemiology and Risk Factors

Although the incidence of testicular torsion in only 4.5 in 100,000 males aged 1 to 25 years (16), testicular torsion is the third most common cause of malpractice lawsuits in adolescent males aged 12 to 17 years (17). This is because it is misdiagnosed in up to 12.5% of initial encounters (18). The most common misdiagnosis is epididymitis.

Testicular torsion occurs in a bimodal distribution. The first, which only includes a small number of cases, occurs in the neonatal period. The second curve, which accounts for 65% of all torsions (19), occurs in the peripubertal period. Predisposing factors include congenital anatomic abnormalities. It is important to note that previous orchiopexy does not significantly decrease future risk of torsion, so do not lower your suspicion of torsion in a patient with prior testicular surgery.


Each testis is surrounded by a layer of tissue called the tunica vaginalis, which consists of both a visceral and a parietal layer. In most cases, the testis is posteriorly anchored to the tunica. However, in 12% of males, the testis is suspended freely within the tunical cavity via the spermatic cord, so the testes are prone to rotate along the axis of its cord. This congenital predisposition to testicular torsion is known as the “bell-clapper deformity” (19).

The pathophysiology of testicular torsion varies slightly depending on whether the event happens during the neonatal period versus the peripubertal period. In newborns, the testes and their surrounding tissue are extremely mobile, so the cord and the tunica vaginal twist as a unit, resulting in “extravaginal torsion.” As males age and the tunica becomes less mobile, the testis is more prone to twist within its covering. This is known as “intravaginal torsion.”

Torsion usually occurs in the absence of a preceding event. It commonly occurs during sleep, when unilateral cremasteric muscle contraction results in asymmetric movement of the testis within the tunica vaginalis (20). Because the cremasteric muscle fibers are wrapped around the spermatic cord, they are able to move the testis up and out of the scrotum. If the torsion results in twisting of cremasteric fibers, the cremasteric reflex will be absent on that side (21). In addition, testicular torsion leads to reflex stimulation of the celiac ganglion, which results in significant nausea and vomiting.

Testicular torsion is a surgical emergency because the twisted spermatic cord results in obstruction of both the venous and arterial vessels. This lack of blood flow can lead to rapid necrosis of the testicle; thus, any male (especially pubertal/prepubertal) with testicular pain or swelling must be regarded as torsion until proven otherwise (22)!

Clinical Presentation

Testicular torsion classically presents with acute testicular pain, nausea, and vomiting. Sudden onset pain is highly suggestive of testicular torsion, but remember that other etiologies, such as epididymitis, may present with pain that is similar in onset and character. In addition, up to 16% of patients with testicular torsion experience a gradual onset of pain (23). Pain may be localized to the testis, but it may also be generalized abdominal pain, especially in patients with an undescended testis. In a study of 597 patients, 5% of patients with testicular torsion and a fully descended testicle did not describe any scrotal pain, and 22% had abdominal pain that preceded and exceeded the scrotal pain (27). Approximately 36% of patients had a history of previous unilateral or bilateral testicular pain or swelling (27).

The pain associated with testicular torsion is usually unprovoked. One study found that injury was implicated in only 4% of cases, recent exercise in 7%, and bicycle riding in 3% (19). Close to 11% were woken from sleep with the pain.

Nausea and vomiting is present in up to 70% of patients with testicular torsion (24), and the combination of scrotal pain or swelling and nausea or vomiting increases likelihood of testicular torsion compared to similar etiologies, like epididymitis or torsion of a testicular appendage. Dysuria and other urinary symptoms are rare in testicular torsion (5%) and are more consistent with epididymitis.

Several studies suggest that presence of pain of duration less than 24 hours, nausea/vomiting, high position of the testis, and abnormal cremasteric reflex have a high positive prognostic value for testicular torsion (20,21,28). One study found that all of the patients with testicular torsion had at least one of the four risk factors, while none of the children with the absence of the four risk factors were diagnosed with torsion (17). Testicular appendageal torsion presents similarly to testicular torsion but usually lacks the systemic symptoms of nausea and vomiting (20).

Because testicular torsion has a relatively nonspecific clinical presentation, and because young boys are often unable to accurately characterize their pain, testicular torsion may present with vague symptoms, sometimes in a manner similar to gastroenteritis (19). Thus, always consider testicular torsion in the differential diagnoses of any male presenting with abdominal pain or vomiting!

Physical Exam

Vital signs are often normal in patients presenting with early testicular torsion. In fact, mild fever and tachycardia are late signs, associated with low testicular salvage rates (19).

The most common physical exam finding is swelling and erythema of the affected hemiscrotum, which is seen in up to 80% of cases (21). Testicular tenderness (60%) and a high-riding testis (50%) with a “transverse lie” (30%) are other common findings (21,19). Although absent cremasteric reflex is an element of the classic description of testicular torsion, the prevalence in the literature ranges from 21% (21) to 100% (22). Therefore, absent cremasteric reflex is not sensitive enough to be a reliable physical exam finding. In addition, up to 30% of males with normal testicles lack a cremasteric reflex.

Another potentially misleading physical exam finding is epididymal tenderness, which may be present in approximately 16% of patients with confirmed testicular torsion (29). The physical exam can be deceptively consistent with epididymitis, which is why it is important to maintain a high level of suspicion for any male with testicular pain, especially in adolescent boys with abdominal, scrotal, or testicular pain.


It is not possible to consistently and accurately differentiate testicular torsion from epididymitis and other scrotal pathologies by physical exam alone (22). In addition, lab tests are usually not useful in the diagnosis of testicular torsion. It is reasonable to obtain a urine sample in patients with suspected torsion, because a urinalysis is almost always normal in testicular torsion. Evidence of infection or pyuria is more consistent with other etiologies of scrotal pain (21).

Ultrasound with color-flow duplex is the imaging modality of choice to diagnose testicular torsion. Findings that indicate the presence of torsion include reduced or absent blood flow to the affected testicle. Absence of blood flow is diagnostic for torsion, with specificity close to 100%. However, the sensitivity ranges from 69-90% (23), and several recent studies found sensitivities of approximately 82% (24). There are several reasons for this. First, a partial torsion may reveal falsely reassuring blood flow. Additionally, in a testicle with torsion-detorsion pathology, the blood flow may actually appear normal or increased.  Three aspects of the US should be evaluated: gray scale appearance (desiring similar findings between the testicles), visualizing arterial and venous blood flow, and finding low resistance in arterial Doppler.

Because ultrasound is not a reliable diagnostic tool, many investigators have researched alternative methods for diagnosing testicular torsion. In the TWIST (Testicular workup for ischemia and suspected torsion) study, Barbosa and colleagues attempted to make a scoring system to risk-stratify for testicular torsion (30). The score assigns points to physical exam findings and historical factors: nausea/vomiting (1 point), presence of testicular swelling (2 points), hard testicle (2 points), absent cremasteric reflex (1 point), and high-riding testis (1 point). According to this study a score greater than 5 is highly indicative of testicular torsion and the patient should go straight to the OR without imaging. Per the study, a patient with a score less than two has low risk for torsion and thus does not require ultrasound. Patients with a score between 2 and 5 are considered “indeterminate” and require ultrasound. The TWIST score reduces ultrasound use by 20%, and it is 100% sensitive for testicular torsion. However, it is not widely accepted, in part because it has not been validated. Nonetheless, it emphasizes an important point: because ultrasound lacks sensitivity for testicular torsion, the diagnosis is largely clinical! Do not delay surgical intervention to obtain confirmatory imaging (20).


The most definitive diagnostic and treatment modality for testicular torsion is detorsion of the affected testicle.

If clinical suspicion for torsion is high, you may attempt to manually detorse in the emergency department (25). Most testicular torsions occur in a lateral-to-medial direction, so the “open-book method” is preferred. This involves rotating the affected testicle 1½ full rotations medial-to-lateral. The endpoint of successful detorsion is resolution of pain. If pain increases with rotation, it is likely that you are worsening the torsion, so attempt the same maneuver in the lateral-to-medial direction. Consult urology regardless of whether manual detorsion appears successful.

If torsion is suspected and manual detorsion is unsuccessful, consult urology for emergent surgical intervention. The classic “golden window” for surgical intervention of testicular torsion is six-hours (19), because testicular preservation rates were once thought to rapidly decline after six hours of torsion symptoms. However, recent literature suggests that viability may extend well-beyond this window. Thus, do not lessen the urgency of your surgical consult if symptoms have persisted for 8, 12, or even 24 hours! Many pediatric urologists advocate for aggressive surgical intervention in suspected testicular torsion, as the risks of missing a torsion include infertility, sepsis, and death; however, the risks of performing an unnecessary surgery are comparatively low (31).

Case 3:

A 24-year-old female presents with sudden-onset, right lower quadrant abdominal pain with associated nausea but no fever, vomiting, or diarrhea. Her vital signs are normal, and her exam is remarkable for right lower quadrant tenderness to palpation. Pelvic exam is unremarkable except for mild right adnexal tenderness.


Epidemiology and Risk Factors

The exact prevalence and incidence of ovarian torsion are unknown. However, up to 3% of women who present to the emergency department with acute abdominal pain have adnexal torsion (32). While infantile and childhood torsion is possible, it is very rare in the prepubertal period. Nearly ¾ of all cases of ovarian torsion present during the reproductive years, from 20-40 years old (33). Risk factors include ovulation induction, ovarian hyperstimulation syndrome, history of adnexal torsion, PCOS, previous tubal ligation, and pregnancy (34). Malignancy may be associated with ovarian torsion in 1.1-2% of adult patients, and the incidence of malignancy in children is even lower (33). In a retrospective chart review involving 87 women with diagnosed ovarian torsion, 35% had prior pelvic surgery (21% of these were tubal ligation), and 22% had a known history of ovarian cyst (35).

The most significant risk factor for ovarian torsion is the presence of a large ovarian cyst or mass, which predisposes the ovary to twisting. In adults, a causative finding for adnexal torsion is found in 64-82% of cases (38,39). In pediatric patients, the incidence of underlying ovarian pathology ranges from 51-84% (36,37).  The risk of ovarian torsion correlates with the size of an ovarian cyst. The risk is higher for cysts greater than 4-5 cm in diameter (33).

However, adnexal torsion may occur in patients with no underlying adnexal pathology (38). One study found that up to 46% of torsion cases involve normal-appearing ovaries (41).


Whether due to ovarian enlargement, cyst, or just an over-mobile ovary, ovarian torsion occurs when the ovary twists along the axis of the adnexa (40). This leads to the blockage of venous return, which results in congestion and ultimately decreased arterial blood flow. Once the arterial blood flow is compromised, the ovary is in danger of ischemia and necrosis.

Ovarian torsion is significantly more likely to occur on the right side, with a ratio of approximately 3:2 (42). This may be due to a longer utero-ovarian ligament on the right side, or the presence of the sigmoid colon on the left side, which limits mobility of the adnexa (33).

Clinical Presentation

Ovarian torsion classically presents with sudden-onset pain, concomitant with the onset of nausea and vomiting, followed by persistent colicky pain (33,40). Up to 90% of patients report acute onset abdominal pain, usually isolated to one side (44). The pain may be constant, or (in the case of torsion/detorsion) intermittent. One meta-analysis found the pain in ovarian torsion to be sudden onset (59%), sharp or stabbing (70%), and radiating to flank, back, or groin (51%) (33). If prompted, most patients report a history of similar pain, suggesting the possibility of intermittent ovarian torsion.

Other symptoms include nausea (70%), vomiting (45%), and fever (20%). If an adnexa becomes necrotic, the patient may exhibit peritoneal signs, which are both rare and a poor prognostic indicator (42).

Children with ovarian torsion have less severe symptoms and are less likely to present with nausea and vomiting (33). In addition, because the ovaries are relatively higher and intra-abdominal in girls compared to women, the clinical presentation is often vague in children.

Thus, it is important to consider ovarian torsion in all female patients presenting with abdominal or pelvic pain, nausea, and vomiting. Sounds easy enough, right? Because nothing else presents with those symptoms. Except appendicitis, diverticulitis, nephrolithiasis, incarcerated hernia, mesenteric adenitis, gastroenteritis, ruptured ovarian cyst, PID, tubo-ovarian abscess, ectopic pregnancy…and the list goes on. The vague symptoms and extensive differential diagnosis for ovarian torsion are two reasons that ovarian torsion is a commonly missed diagnosis! One study found that ovarian torsion was considered in the admitting differential in only 47% of patients with confirmed ovarian torsion. Other studies demonstrate that adnexal torsion was diagnosed preoperatively in only 37-50% of cases (44,45). Despite the diagnostic conundrum that ovarian torsion provides, there are no scoring systems or risk stratifying tools that help make the diagnosis (46). Maintain a high clinical suspicion for all women with undifferentiated abdominal or pelvic pain.

Physical Exam

Unfortunately, the physical exam does not help make the diagnosis more obvious. Vital signs are usually normal, with a low-grade fever (18%) in some cases, and perhaps slight tachycardia with elevated blood pressure if the pain is severe (42).

The rest of the exam is also non-specific. The most common finding is unilateral lower abdominal tenderness. However, up to 30% of patients may have no pain on exam (35)! The pelvic exam may reveal a palpable adnexal mass, but up to 75% of patients with proven adnexal torsion do not have a palpable mass (43).


Labs are useful when considering ovarian torsion, only because they may offer a suitable alternative diagnosis. Obtain a urinalysis, pregnancy test, CBC, and electrolyte panel. Urinalysis may demonstrate sterile pyuria, and up to 50% of patients with ovarian torsion have slight leukocytosis on CBC (46).

Ultrasound is currently the most utilized diagnostic tool. “Positive” findings include a significant (greater than 4 cm) ovarian mass, free fluid in the cul-de-sac, unilateral ovarian enlargement, and decreased blood flow in the affected ovary (46). However, just as ultrasound is specific but not sensitive in diagnosing testicular torsion, the diagnostic yield is questionable in ovarian torsion. Specificity is as high as 92%, but sensitivity is likely as low as 40% (47). Normal Doppler flow is present in 45-61% of cases (26).

Ultrasound has traditionally been preferred over CT imaging in the case of suspected ovarian or endometrial pathology. However, recent research has focused on the use of CT in this setting. One review article posits that CT is more sensitive than ultrasound for detecting underlying adnexal masses, and just as sensitive as ultrasound in finding torsion (48). The data on this topic are conflicting: some studies demonstrate a distinct advantage of ultrasound over CT, some an advantage of CT over ultrasound, and still other studies demonstrate equal efficacy for both imaging modalities. Regardless of which imaging modality is superior, ovarian torsion is sometimes diagnosed by CT scans ordered for suspected appendicitis or other diagnoses. CT has a high enough specificity that when CT demonstrates findings of ovarian torsion, and the performance of another imaging exam (i.e. US) that delays therapy is unlikely to improve preoperative diagnostic yield.


The only effective treatment for ovarian torsion is surgical intervention. Laparoscopic surgical evaluation of the ovaries is also the golden standard for diagnosis, because diagnostic imaging is considered unreliable. Unlike surgery for testicular torsion, which often cannot salvage the affected testicle, urgent surgical detorsion successfully preserves ovarian function in over 90% of cases (49).


This is the second in a two-part series on surgical emergencies: conditions that require quick disposition and potentially time-sensitive emergent surgery. These diseases include ruptured ectopic pregnancy, AAA, aortic dissection, necrotizing fasciitis, and ovarian / testicular torsion. You must maintain a high index of suspicion for these diseases, as delay in treatment can lead to substantial increases in morbidity and mortality. In all of these disease processes, hemodynamic instability = emergent surgical consultation.



-Consider this diagnosis in any patient with cellulitis, but especially in patients with diabetes and obesity.

-Laboratory testing and imaging do not have high enough sensitivity to reliably exclude the diagnosis, so this is truly a clinical diagnosis!

-Necrotizing fasciitis spreads as quickly as 1 inch per hour. Its mortality is as high as 35% and is directly related to time-to-treatment.

Antibiotics should be initiated immediately, but antibiotics alone are not an effective treatment; emergent surgical exploration is necessary.

-Must consider in any peripubertal male with abdominal pain +/- nausea and vomiting.

-Classic exam findings include swelling and erythema of the affected hemiscrotum, with unilateral loss of the cremasteric reflex, and testicular tenderness.

-The most common imaging modality to diagnose testicular torsion is Doppler ultrasonography, but this is an unreliable diagnostic tool, so if your suspicion for testicular torsion is high, then act quickly regardless of ultrasound results!

-You may attempt to manually detorse in the ED by rotating the testicle in a medial-to-lateral direction. Resolution of pain is an indicator of successful detorsion.

-Even if manual detorsion is successful, an emergent urology consult is necessary!



Maintain a high clinical suspicion for all women with undifferentiated abdominal or pelvic pain.

-Most common in the reproductive years (20-40 years old).

-Ovarian torsion classically presents with sudden-onset, unilateral pain, concomitant with the onset of nausea and vomiting.

Ultrasound is the most commonly used imaging modality, but CT or MRI may be equally efficacious. Ovarian torsion may not be detectable by any imaging if there is torse/detorse pathology.

-The only effective treatment is surgical intervention, which successfully preserves function in 90% of cases.


References/Further Reading:

  1. Oud, L., Watkins, P. Contemporary trends of the epidemiology, clinical characteristics, and resource utilization of necrotizing fasciitis in Texas: a population-based cohort study. Critical care research and practice. 2015.
  2. Arif N, Yousfi S, Vinnard C. Deaths from necrotizing fasciitis in the United States, 2003–2013. Epidemiology and infection 2016; 144(6): 1338-1344.
  3. Stevens DL et al. Practice Guidelines for the diagnosis and management of skin and soft-tissue infections: IDSA Guidelines. Clinical Infectious Diseases 2005; 41: 1373-1406.
  4. Kelley EW and Magilner D. Soft tissue infections. In Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. New York: McGraw-Hill, 2016. 1034-1036.
  5. Park SJ, Kim DH, Choi CI, Yun SP, Kim JH, Seo H, J HJ, Jun TY, Necrotizing soft tissue infection: analysis of the factors related to mortality in 30 cases of a single institution for 5 years. Ann Surg Treat Res 2016 Jul; 91(1): 45-50.
  6. Hakkarainen TW, Kopari NM, Pham TN, et al. Necrotizing soft tissue infections: review and current concepts in treatment, systems of care, and outcomes. Current Problems in Surg. 2014; 51: 344-362.
  7. Wong CH, Khin LW, Heng KS, Tan KC, Low CO. LRINEC score (The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue infections. Crit Care Med 2004 Jul; 32(7): 1535-41.
  8. Su YC, Chen HW, Hong YC, Chen CT, Hsiao CT, Chen IC. Laboratory Risk indicator for necrotizing fasciitis score and the outcomes. Anz Journal of Surgery Nov 2008; 78(11): 968-972.
  9. Burner E, Henderson SO, Burke G, Nakashioya J, Hoffman JR. Inadequate Sensitivity of the Laboratory Risk Indicator to Rule Out Necrotizing Fasciitis in Emergency Department Patients. Western Journal of Emergency Medicine 2016 Apr 26.
  10. Raam R, Moran GJ, Jhun P, Herbert M. Worms and Flesh-Eating Bacteria? The Worst Day of Your Life. Annals of Emergency Medicine 2016 Aug; 68(2): 245-8.
  11. Wilson MP, Schneir AB. A case of necrotizing fasciitis with a LRINEC score of zero: clinical suspicion should trump scoring systems. J Emerg Med 2013; 44: 928–931.
  12. DL Stevens et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clinical Infectious Diseases 2014; 59: e10–52.
  13. Goh T, Goh LG, Ang CH, Wong CH. Early diagnosis of necrotizing fasciitis. BJS 2014 Jan; 101(1): e119-125.
  14. Castleberg, E., Jenson, N., & Dinh, V. A. (2014). Diagnosis of Necrotizing Fasciitis with Bedside Ultrasound: the STAFF Exam. Western Journal of Emergency Medicine, 15(1), 111–113.
  15. Wong CH, Chang HC, Pasupathy S, et al. Necrotizing fasciitis: clinical presentation, microbiology, and determinants of mortality. J Bone Joint Surg Am Volume 2003; 85: 1454-1460.
  16. Mansbach JM, Forbes P, Peters C. Testicular torsion and risk factors for orchiectomy. Arch Pediatr Adolesc Med. 2005; 159(12): 1167-1171.
  17. Selbst SM, Friedman MJ, Singh SB. Epidemiology and etiology of malpractice lawsuits involving children in US emergency departments and urgent care centers. Pediatr Emerg Care 2005; 21(3): 165-169.
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  19. Cuckow PM, Frank JM. Torsion of the testis. BJUI August 2000; 86(3): 349-353.
  20. Davis JE. Male genital problems. In Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. New York: McGraw-Hill, 2016. 605-607.
  21. Boettcher M., Bergholz R, Krebs TF, Wenke K, Aronson, DC. Clinical predictors of testicular torsion in children. Urology 2012; 79(3): 670-674.
  22. LB Mellick. Torsion of the testicle: It is time to stop tossing the dice. Ped Emerg Care. January 2012; 28(1): 80-86.
  23. Boettcher M, Krebs T, Bergholz R, Wenke K, Aronson D, & Reinshagen K. Clinical and sonographic features predict testicular torsion in children: a prospective study. BJU International 2013; 112(8): 1201-1206.
  24. Ciftci AO, Senocak ME, Tanyel FC, Buyukpamukcu N. Clinical Predictors for differential diagnosis of acute scrotum. Eur J Pediatr Surg 2004; 14(5), 333-338.
  25. Melekos M, Asbach H, Markou S. Etiology of the acute scrotum with regard to age distribution. J Urol 1988; 139: 1023-1025.
  26. Cass AS, Cass BP, Veeraraghavan K. Immediate exploration of the unilateral acute scrotum in young male subjects. J Urol 1980; 124(6): 829-832.
  27. Anderson JB, Williamson RC. Testicular torsion in Bristol: a 25-year review. Br J Surg 1988; 75(10): 988-992.
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