A female aged 13 years with morbid obesity and recent hospitalization for pyelonephritis presents with abdominal pain, tachycardia, and shortness of breath. What's the diagnosis?
A female aged 13 years with morbid obesity (body mass index, 56.7 kg/m2) and recent hospitalization for pyelonephritis presented to the pediatric emergency department with abdominal pain, tachycardia, and shortness of breath. She completed a course of oral antibiotics for the pyelonephritis about 4 days prior and initially felt well. Two days later, she started to experience diffuse abdominal pain accompanied by nonbloody, nonbilious emesis and watery diarrhea. The patient also complained of increased thirst and new bowel and bladder incontinence. That morning she developed difficulty breathing with tachypnea and a generalized feeling of weakness, which prompted her presentation to the pediatric emergency department. She denied fever, dysuria, or malodorous urine since completing the above antibiotics. She also denied being sexually active. She had operative pinning for a slipped capital femoral epiphysis about 3 months earlier, for which she has no residual pain or swelling, but she still uses crutches and has been sedentary since the procedure.
Triage vital signs show a temperature of 36.6 °C with a heart rate of 177 beats per minute; blood pressure, 104/84 mmHg; respiratory rate, 30 breaths per minute; pulse oximetry, 98% on room air; and capillary refill time of 3 seconds. She is generally ill appearing and moaning in pain. Her exam is also notable for dry mucous membranes and otherwise significant for tachycardia without murmurs, tachypnea with clear breath sounds, and a soft and nondistended but diffusely tender abdomen. She has no rashes, joint swelling, or swelling of lower extremities.
Immediate interventions to treat the tachycardia and early signs of shock include intravenous (IV) fluid resuscitation with improvement in heart rate, cap refill time, and blood pressure. A blood culture was drawn followed by administration of empiric IV ceftriaxone and metronidazole. Antibiotics were selected for broad-spectrum coverage in this patient who fits systemic inflammatory response syndrome criteria and for additional polymicrobial coverage for possible intra-abdominal infection (Table 1). An electrocardiogram (ECG) was obtained to evaluate for right heart strain, and ischemia was notable for sinus tachycardia. Computed tomography angiogram (CTA) of chest and CT abdomen/pelvis with IV contrast imaging were ordered.
Given the patient’s ill appearance, abnormal vital signs, and multiple sources for possible infection, the following broad laboratory work-up was pursued. An initial glucometer reading was 119 mg/dL. Additional results returned as follows: complete blood count with leukocytosis of 30 K/mm3 with 8% bands; hemoglobin, 10.7 g/dL, hematocrit, 33.6 g/dL, platelets, 649 K/ mm3; C-reactive protein, 56 mg/dL (<0.5 mg/dL); lactate, 2 mmol/L (normal <2.3 mmol/L). D-dimer was elevated at 19 mg/L FEU (normal <0.5 mg/ dl FEU). A comprehensive metabolic panel, venous blood gas, troponin, lipase, urinalysis, and urinary pregnancy test were all within reference range.
The greatest initial concern and most immediately life-threatening diagnosis was a pulmonary embolus (Table 2). Although less common in the pediatric than adult population, the patient had several risk factors, including obesity, minimal ambulation for the past several months, surgical procedure, and recent hospitalization. A high index of suspicion is also needed for patients on oral contraceptive therapy, recent travel, malignancy, or a family history of hypercoagulability. The physical exam of acute distress, tachypnea with clear breath sounds, and significant tachycardia supported this possibility. No unilateral leg pain or swelling was seen, although this can be difficult to assess in patients with an obese body habitus. Patients typically present with chest pain, but abdominal discomfort can also be referred. ECG findings may be normal or demonstrate sinus tachycardia, right bundle branch block, ST-segment elevation in V1 and aVR, and low amplitude QRS complexes. The Simplified Wells Score and Pulmonary Embolism Rule-Out Criteria (PERC) are often used to risk- stratify patients with possible pulmonary embolism. The Wells Score rates patients on symptoms, likelihood of diagnosis, and history of hypercoagulability; patients with more than 1 risk factor should have immediate imaging. Those with a score of 1 or less can then be further assessed via PERC. PERC applies some of the same factors as Wells and also accounts for medication use and physical exam. If there are no PERC criteria met in addition to a Wells score of less than 2, no further evaluation is indicated. If any PERC signs are present, further stratification with D-dimer testing is suggested. Although this can be helpful to supplement clinician decision-making, both have not been validated for patients less than 18 years old. Thus, these should be used only as a guide and not to replace physical exam and clinical suspicion.
Although the patient had no reported fevers, sepsis must always be considered in a patient with persistent tachycardia. She had many possible intra-abdominal sources for sepsis, most notably a recurrent pyelonephritis complicated by a renal abscess. Her body habitus limited physical exam localization of pain to a specific abdominal quadrant; additional possible etiologies include cholecystitis, pancreatitis, appendicitis, and tubo-ovarian abscess (TOA). Other infectious sources are a lower lobe pneumonia with diaphragmatic irritation resulting in abdominal pain or an osteomyelitis from her recent hip surgery requiring hardware placement. Her vital sign improvement with IV fluid resuscitation, the significant leukocytosis with increased bands, and her elevated inflammatory markers further supported an active infection as the diagnosis. The elevated D-dimer indicated a possible blood clot, but this is also a nonspecific finding and usually elevated in sepsis, as well. The treatment of suspected sepsis includes IV fluid hydration and early broad-spectrum antibiotics following collection of all relevant cultures. If patients have hemodynamic instability despite aggressive fluid resuscitation, the vasoactive agent of choice according to recently updated pediatric sepsis guidelines is norepinephrine or epinephrine.1
Hyperosmolar hyperglycemic state
A history of new onset polydipsia and urinary incontinence raised the suspicion of an endocrine etiology. Although the patient was an adolescent, her body habitus suggested an increased risk of type 2 diabetes mellitus with resulting hyperosmolar hyperglycemic state (HHS). HHS is a consequence of hyperglycemia, significantly elevated serum osmolarity, and severe dehydration. It is typically a complication of uncontrolled type 2 diabetes or may be triggered by an underlying infection leading to dehydration. It can lead to fatal cerebral edema and cardiovascular collapse. HHS is diagnosed by clinical findings of dehydration, lethargy, and altered mental status. Laboratory evaluation includes elevated glucose greater than 600 mg/ dL, elevated plasma osmolarity of 320 mOsm/L or higher, and no ketoacidosis.2 Management requires aggressive IV hydration at twice the maintenance rate and administration of only subcutaneous insulin rather than a continuous infusion.
Unexplained tachycardia in the pediatric population may also indicate myocarditis. Myocarditis is an inflammation of the cardiac muscle usually caused by a recent viral infection. Additional signs and symptoms include tachypnea, fatigue, vomiting, hepatomegaly, and an S3 gallop on exam. ECG may show sinus tachycardia and elevated ST segments. Lab work-up usually is associated with an elevated troponin. A chest x-ray may show an enlarged cardiac silhouette and pulmonary edema. Patients typically do not tolerate IV fluids well and should be emergently transferred to a facility with pediatric cardiology services.
Radiographic testing revealed the diagnosis of the patient. A CTA chest was negative for pulmonary embolus, and the CT abdomen/ pelvis with and without IV contrast demonstrated a large fluid collection in the right lower quadrant (Figure) that was most consistent with a TOA. There was also extensive reactive bowel inflammation that likely caused her associated diarrhea and incontinence.
Upon diagnosis of TOA, general pediatric surgery service was consulted. The patient was admitted to the pediatric intensive care unit following the surgical procedure. Pediatric infectious disease and gynecology services were consulted to guide IV antibiotic therapy. Antibiotics were then further broadened to vancomycin and piperacillin-tazobactam. Blood cultures remained negative. Her intra-abdominal culture grew multiple organisms. Gonorrhea and chlamydia polymerase chain reaction were negative. The patient had a prolonged hospital course of several weeks. She required 2 additional operative interventions for repeat drain placement and ultimately a right salpingectomy. She was discharged with multidisciplinary follow-up, including physical therapy and weight loss clinic. The patient continuously denied any sexual activity or sexual abuse. Her infection was attributed to a combination of recent urinary system infection and poor genitourinary hygiene.
TOA is an intra-abdominal infection that usually results as a late complication of pelvic inflammatory disease (PID). It typically presents with abdominal pain, vaginal discharge, adnexal mass, and leukocytosis in sexually active females of reproductive age. Up to 50% of infected patients may be afebrile with an ill appearance. As the infection is caused by ascension of bacteria from the lower genital tract, etiology of micro-organism is usually polymicrobial.3 The predominant cause is anaerobic bacteria rather than Neisseria gonorrhoeae or Chlamydia trachomatis. Organisms include Escherichia coli, Bacteroides fragilis, other Bacteroides species, Peptostreptococcus, Peptococcus, and aerobic streptococci.3 Risk factors for TOA are reproductive age, intrauterine device use, multiple sexual partners, and past PID infections.
Physical exam usually notes pelvic tenderness, often with evidence of peritonitis. Bimanual exam may re- veal cervical motion tenderness and adnexal tenderness and/or mass. Radiographic testing will confirm the diagnosis, and multiple modalities are acceptable including ultrasonography, CT scan, and MRI.
Although TOA is almost always caused by further ascension of bacteria from PID, it can result spontaneously without history of sexual activity and as a complication of hysterectomy. In the pediatric population, it has been rarely seen as a sequela of inflammatory bowel dis- ease. There are also case reports of TOA in adolescents resulting from a combination of obesity, constipation, recurrent urinary tract infection, and poor hygiene.4,5
After initial recovery, later complications include chronic pelvic pain, infertility, ectopic pregnancy, ovarian vein thrombosis, and recurrent PID.
TOA can be managed both medically and surgically. All patients should be admitted to the hospital with a gynecology consult. If the TOA has not yet ruptured, antibiotics can be trialed.6 The initial recommended regimen includes IV cefotetan or IV cefoxitin and IV doxycycline, IV ampicillin with IV gentamicin loading dose followed by IV clindamycin, or IV ampicillin-sulbactam and IV doxycycline. IV medications can be transitioned to oral once patients have defervesced, resolution of leukocytosis, clinical improvement in pain, and improvement in size of abscess on imaging.
Surgery may be pursued as source control for unstable patients, large abscess size, or failure of antibiotics. If patients have worsening symptoms or no improvement after 2 weeks of oral therapy, surgery is recommended. Surgical options include intervention- al radiologic percutaneous drainage or laparoscopy/laparotomy for drainage and possible salpingectomy.6
Given the significant associated complications, TOA prevention is important when it comes to adolescent health. Health care team members should counsel patients on safe sex practices, PID, and TOA risk factors before a patient develops these conditions.
1. Weiss SL, Peters MJ, Alhazzani W, et al. Surviving sepsis campaign international guidelines for the management of septic shock and sepsis-associated organ dysfunction in children. Pediatr Crit Care Med. 2020;21(2):e52-e106. doi:10.1097/PCC.0000000000002198
2. Adeyinka A, Kondamudi NP. Hyperosmolar hyperglycemic nonketotic coma. National Center for Biotechnology Information. StatPearls. Accessed August 4, 2021. https://www.ncbi.nlm.nih.gov/books/NBK482142/
3. Curry A, Williams T, Penny ML. Pelvic inflammatory disease: diagnosis, management, and prevention. Am Fam Physician. 2019;100(6):357-364.
4. Chernick LS. Tubo-ovarian abscesses in nonsexually active adolescents: A rare but consequential miss. J Adolesc Health. 2019;65(2):175-176. doi:10.1016/j.jadohealth.2019.04.006
5. Hartmann KA, Lerand SJ, Jay MS. Tubo-ovarian abscess in virginal adolescents: exposure of the underlying etiology. J Pediatr Adolesc Gynecol. 2009;22(3):e13-e16. doi:10.1016/j.jpag.2008.03.006
6. Jiang X, Shi M, Sui M, Wang T, Yang H, Zhou H, Zhao K. Clinical value of early laparoscopic therapy in the management of tubo-ovarian or pelvic abscess. Exp Ther Med. 2019; 18(2):1115-1122. doi:10.3892/etm.2019.7699