The Case Files
Welcome to the Case Files!
The Case Files is an anecdotal collection of emergency medicine cases to enable physicians and researchers to find clinically important information on unusual conditions.
Case reports should focus on:
- Unusual side effects or adverse interactions.
- Unusual presentations of a disease.
- Presentations of new and emerging diseases, including new street drugs.
- Findings that shed new light on a disease or an adverse effect.
Comment on a case or submit your own case following the instructions in the Submissions box to the right.
Tuesday, December 09, 2014
By Brian Ichwan, MD & Andrew King, MD
A 35-year-old woman with a history of congenital hydrocephalus with bilateral ventriculoperitoneal (VP) shunts, morbid obesity, and a ventral hernia after multiple abdominal surgeries presented to the ED with three weeks of abdominal pain and distention that had acutely worsened over the previous two days. Her vital signs revealed a temperature of 100.4°F, blood pressure of 107/60 mm Hg, pulse rate of 118 bpm, and oxygen saturation at 95%. Her exam was significant for a large ventral hernia with a large exquisitely tender area of erythema and necrosis with bulla formation. (Figure 1.)
She was emergently transferred to an associated Level I trauma center for direct admission with general surgery for her sepsis with a suspected necrotizing soft tissue infection (NSTI). She was started on IV vancomycin and cefepime, IV resuscitation, and pain medication in the ED. Her initial blood work showed WBC 27.9, lactate 3, BUN 26, and creatinine 2.13.
The time from initial assessment in the tertiary ED to the academic hospital OR was six hours. The patient underwent an exploratory laparotomy with incision and drainage. Multiple large and small bowel fistulas were found secondary to a necrotic incarcerated bowel in the ventral hernia, which was complicated with an adherent VP shunt at the abdominal end. She was admitted to the surgical ICU and underwent four additional surgeries during her admission for multiple small and large bowel resections, abdominal wall resections, VP shunt externalization, and right ventriculopleural shunt placement.
Antibiotics were broadened to piperacillin/tazobactam and vancomycin, which were subsequently narrowed to ertapenem after cultures grew Bacteroides, Prevotella, Klebsiella, and alpha-hemolyticStreptococcus. The patient ultimately recovered well with neurologic stability, and was discharged to a long-term acute care facility with complications, including having 70 percent of her abdominal wall and skin excised (Figure 2), multiple enterocutaneous fistulas, and a ventriculopleural shunt.
Necrotizing soft tissue infections occur by direct microbial invasion of the subcutaneous tissues by trauma or direct inoculation. The cause in this case was direct inoculation via perforated viscous. (J Am Coll Surg2009;208:279.) It is a rare disease with an incidence of approximately 1,000 cases per year in the United States but a morality of greater than 25 percent. (Arch Surg 2005;140:151.)
The most common etiology of NSTI is polymicrobial, which includes anaerobic, gram-negative, and gram-positive cocci. Depending on the organism, multiple different exo- and endotoxins are produced, all resulting in tissue ischemia and liquefactive necrosis that allows for accelerated soft tissue invasion. This local necrosis leads to thrombosis of a large number of capillary beds because of the local hypercoagulability, platelet plugging, and increased interstitial pressure that synergistically act to decrease end tissue perfusion. (Curr Opin Crit Care 2007;13:433.) The thrombosis of perforating vessels to the skin is the key sign found in necrotizing soft tissue infections. These signs may give the unseasoned physician a false sense that there is no urgency to the situation because the underlying soft tissue infection is usually much wider than shown on the surface because large numbers of capillary beds must fail before necrotic skin changes manifest.
NSTI of the abdomen secondary to strangulated bowel perforation is extremely rare, with almost all occurring post-operatively. (Hernia2003;7:220.) One case of NSTI on a lower extremity secondary to a perforated inguinal hernia was reported, and a handful of case reports have been reported on perforations causing NSTI, including rectal cancer, diverticulitis, and trauma. (Hernia 2011;15:571; J Plast Reconstr Aesthet Surg 2012;65:1731; J Emerg Med2008;34:95, Singapore Med J 2009;50:e270.) This is the first case to our knowledge of documented abdominal NSTI secondary to hernia not in a post-operative setting.
An NSTI is often misdiagnosed in the early stages, leading to the high mortality rates because of delayed or inadequate treatment. The most common sign includes tender local erythema with edema, which can easily be misdiagnosed as a non-necrotizing cellulitis. A retrospective study found that 86 percent of patients who were discharged with NSTI were initially misdiagnosed as having cellulitis or simple abscess. (Ann Surg 1996;224:672.) The classic presentation is a rapidly decompensating patient with pain out of proportion associated with anxiety and diaphoresis. (Ann Surg 1995;221:558.) Some patients, however, may become insensate to pain as tissue necrosis progresses and desensitizes nerve fibers.
Surgical debridement is the mainstay therapy; antibiotic therapy won't work because of the extensive tissue ischemia inhibiting adequate delivery of antibiotics to the site of infection. A delay in treatment of as little as six to 12 hours has been shown to contribute to high morbidity and mortality. Many patients will develop a massive systemic cytokine response to the large microbial toxin exposure resulting in a systemic inflammatory response syndrome, which can quickly escalate to septic shock and multiorgan dysfunction. (J Bone Joint Surg Br2001;83:709; World J Emerg Surg 2011;6:46.) It is important for EPs to consider NSTI in the differential for skin lesions, including cellulitis and simple abscesses, with emergent and aggressive referral to surgery for debridement, if suspected.
Friday, November 21, 2014
By Ashley Heaney, MD & Andrew King, MD
A 41-year-old woman with a past medical history of chronic low back pain and migraines presented with a headache. She had had a L4-L5 epidural steroid injection performed for her chronic lower back pain, but complained of a headache immediately after the procedure. The headache was in the front of her head and associated with photophobia. She stated that she had multiple epidural steroid injections in the past with no prior post-procedure headache. She denied neck pain, vision changes, extremity numbness, or extremity weakness.
The patient had a temperature of 98.1°F, a pulse of 76 bpm, a blood pressure of 99/63 mm Hg, a respiratory rate of 16 bpm, and an oxygen saturation of 99% on room air. She was alert and oriented. Her speech was fluent, her cranial nerves were intact, and she had full strength in all extremities. She had normal sensation to dull and light touch in all extremity dermatomes, and her neurologic examination was nonfocal. She also had full range of motion of her neck with no meningismus.
A head CT was obtained, and showed pneumocephalus ventral to the pons and medulla. Pneumocephalus was also present throughout the posterior fossa. She received IV Toradol, Valium, Benadryl, and opiate pain medication with only minimal symptom relief. The patient was evaluated by neurosurgery based on the amount of pneumocephalus present on the CT scan. They recommended inpatient observation and symptom control. The patient was placed supine, and provided with supplemental oxygen and pain medications as needed. After three days, her symptoms had significantly improved, and she was able to be discharged from the hospital.
Headache is a frequently encountered chief complaint in the emergency department. Migraine, subarachnoid hemorrhage, dural venous sinus thrombosis, meningitis, subdural hematoma, epidural hematoma, and carotid artery dissection are all diagnoses that every emergency medicine physician must consider when evaluating a patient presenting with headache. Headaches can be the result of procedures, most commonly lumbar punctures. Cephalgia may also result from epidural puncture from injection or anesthesia. At times, pneumocephalus may result from accidental puncture of the dura mater during a procedure. Post-procedural pneumocephalus is not a frequently encountered diagnosis, and it rarely makes the differential diagnosis of headache in the emergency department.
Pneumocephalus is the accumulation of intracranial air. (Clin Neurol Neurosurg 2009;111:309.) There are multiple etiologies of pneumocephalus, the most common being trauma. Other etiologies include craniotomy, injection of air during a procedure, placement of VP shunts, CSF-pleural fistula, nasopharyngeal cancer with invasion of the skull base, nasal sinus surgery with perforation of the skull base, and otogenic causes. Injection of air can occur from accidental dural puncture during epidural anesthesia, during a blood patch procedure, epidural saline infusions, or spinal anesthesia. (Can J Neurol Sci2002;29:278.)
Pneumocephalus can cause a severe headache, and no direct correlation exists between the amount of air and the presence or severity of the headache. (Can J Neurol Sci 2002;29:278.) It has also been shown that increasing the amount of inspired air oxygen concentration decreases the amount of time needed to absorb intracranial air, decreasing the duration of the patient's headache. This study showed that the duration of absorption of 50 ml of air decreased from 5.8 to 1.9 weeks by 40% FiO2 from 1.9 to 0.6 weeks on room air and 100% FiO2, respectively. (Anesthesiology 1996;84:442.)
Several diagnoses should be added to the headache differential diagnosis in the case of a patient receiving recent epidural spinal injections. Post-procedural headache or low-pressure headache, as well as pneumocephalus, should be added to the differential. The patient can be easily placed on a face mask to expedite air resorption, and can be provided symptom control as needed. This patient was successfully managed using supplemental oxygen and analgesia.
Friday, November 21, 2014
By Brian Ault, DO; Rudolph Baldeo, MD; Martin Winick, MD; Ronald Dvorkin, MD; David Levy, DO
A 5-year-old boy presented to the ED with three days of progressive abdominal pain. He had been afebrile with nonbloody, nonbilious vomiting, decreased oral intake, and resultant decreased urination. He was not taking any prescribed medications, nor was he given any medications for his symptoms.
His initial vital signs were blood pressure 102/70 mm Hg; heart rate 130 beats per minute; SpO2 100% on room air; respiratory rate 22 breaths per minute; temperature 36.8°C orally. He looked well and was interactive, playful, and in no distress. His mucous membranes were dry, and his eyes appeared slightly sunken. His abdomen was soft and nontender, and he had normal bowel sounds. His exam was significant for a mobile, nontender 1 cm round mass, 2 cm above the umbilicus. Blood work and an abdominal ultrasound were unremarkable.
An abdominal x-ray was ordered because of the patient's vomiting in the ED, and it revealed a metallic density in the small intestine with bowel dilated proximal to it, which was consistent with a small bowel obstruction. The patient's brother then admitted to witnessing the ingestion of a quarter one week earlier.
A nasogastric tube was placed, the patient was admitted, and gastroenterology and surgery were consulted. A PO trial using a bowel preparation was given. The patient did not tolerate the prep and the coin remained in the same location, so he was taken for an exploratory laparotomy. The terminal ileum and cecum appeared normal. A cystic lesion on the mesenteric side of the ileum appeared to be narrowing the small bowel, identified as a duodenal duplication cyst. Once the structure was removed, the coin passed easily. The patient recovered, and was discharged home four days after surgery.
Foreign body ingestion in children is extremely common. The American Association of Poison Control Centers documented 182,105 foreign body ingestions in children in 1999, with peak occurrences in ages under 6. (Pediatr Ann 2001;30:736; J Okla State Med Assoc2001;94:183.) It is estimated that 40 percent of ingestions in children are not witnessed and that the most common foreign body ingestions are coins. (J Okla State Med Assoc 2001;94:183.) Approximately 1,500 deaths per year are attributed to ingestion of foreign bodies in the United States. However, significant complications resulting from these ingestions occur in less than one percent of cases.
Common sites for obstruction by an ingested foreign body include the cricopharyngeal area, esophagus, pylorus, and ileocecal valve. Regardless of size, shape, composition, or sharpness, the majority does not meet criteria for immediate removal, and should be initially managed conservatively. (Gastrointest Endosc 2011;73:1085 and 2002;55:802.)
This case encourages practitioners to remember that spontaneous passage of an ingested foreign body is not guaranteed. Some 93 to 99 percent of blunt objects passed without intervention in the pre-endoscopy era, and approximately one percent required surgical removal. (Gastrointest Endosc 2002;55:802 and 2011;73:1085.)Today, 10 to 20 percent of pediatric foreign body ingestions are managed with an endoscopy when objects are found prior to passing the duodenum. (Gastrointest Endosc 2002;55:802 and 2011;73:1085.) Objects longer than 3-5 cm may not spontaneously pass in children 1 year of age and older, and gastroenterology consultation is advised. (Gastrointest Endosc2002;55:802 and 2011;73:1085.) Patients who have swallowed blunt, radiopaque objects should be followed with weekly radiography after the object passes the duodenal sweep, and parents should be instructed to watch for the passage of the object in stool. (Gastrointest Endosc 2002;55:802 and 2011;73:1085.) Most objects will pass within four to six days of ingestion, but some may take up to four weeks.
This case demonstrates an extremely rare, often asymptomatic gastrointestinal finding, a duplication cyst, and how a foreign body ingestion led to its discovery. A duplication cyst is a rare, small bowel malformation that varies in location, size, appearance, and symptoms. They were first recognized in 1733, and are usually found on the mesenteric side of the bowel, as in our case. Duplication cysts may communicate with intestines, and can manifest as obstructions, abdominal masses, intussusception, and GI bleeding. (Semin Pediatr Surg 2000;9:135.) The exact pathogenesis is unknown. The two theories focus on aberrant fetal recanalization or vascular abnormalities. (Semin Pediatr Surg 2000;9:135.) Typically, duplication cysts share three characteristics: a coat of smooth muscle, an epithelial lining, and an attachment to part of the alimentary tract. Generally, duplications are cystic or tubular in shape and are more common in men than women. (Semin Pediatr Surg 2000;9:135.)
Monday, November 10, 2014
A 24-year-old man was brought to the ED with lethargy and confusion. His relatives found him lying flat in his room near a strip of tramadol tablets with 10 empty blisters, which meant he ingested 1,000 mg of the drug. They revealed that he had been taking tramadol illegally for five months. The patient received supportive care and cardiac monitoring. The next day, the patient became alert and complained of pain and discomfort in his upper teeth. He did not remember the seizure, but admitted tramadol abuse. His teeth seemed to be normal but were tender on pressure without evident buccal mucosa ecchymosis or laceration. The patient was discharged with advice for dentistry follow-up. A panoramic radiograph sought by the dentistry consultation demonstrated an upper incisor tooth fracture. (Figure 1.)
Seizures have been reported with tramadol even at recommended doses. (Ann Pharmacother 2005;39:1039.) Tramadol poisoning may not be life-threatening, but it may complicate the intoxicated patients if accompanied by seizures. (J Pak Med Assoc 2009;59:178; Eur Rev Med Pharmacol Sci 2012;16[Suppl 1]:34.) Farajidana et al. found the prevalence of trauma in tramadol ingestions was 24.6 percent, mostly in the face (9.5%). It didn’t detail the type of injuries, however. (Eur Rev Med Pharmacol Sci 2012;16[Suppl 1]:34.)
Patients with tramadol-induced seizures are significantly more susceptible to facial and dental injuries, which may remain undetected. It is important for EPs to consider occult oro-dental traumas in tramadol-induced seizures, even when they are unwitnessed. Thorough examination, imaging, and follow-up should be done to rule out or confirm possible injuries.
Dr. Mirakbari is an assistant professor in forensic medicine and toxicology at Bu Ali Hospital, a part of Qazvin University of Medical Sciences in Qazvin, Iran. He completed an emergency medicine research fellowship at the University of British Columbia in Vancouver.
Tuesday, October 14, 2014
By Ichwan, Brian MD; Barrie, Michael MD; Neltner, Kurt MD
A 37-year-old man with no significant medical history presented to the emergency department with a headache. He described it as an insidious, constant severe pain that was initially localized occipital but progressed to a bitemporal distribution. His neurologic exam, extraocular movements, and visual acuity were all normal. The patient was given symptomatic treatment with compazine and Benadryl. He was responsive to therapy and discharged home after his headache symptoms resolved.
Seven days later, however, he presented to the emergency department with a worsening headache, progressive altered mental status, fever, and bilateral proptosis. His temperature was of 103.9°F, blood pressure was 194/82 mm Hg, pulse rate was 87 bpm, and oxygen saturation was 98%. His exam was significant for profound bilateral periorbital edema with significant chemosis, drainage, and overlying erythema. (Figure 1.)
The right eye was impossible to examine because of significant swelling. The extraocular muscles in the left eye were limited in all directions, and pupils were sluggish. Computed tomography without contrast of the head and orbit demonstrated an enlargement of the right superior ophthalmic vein, attenuation of the right sigmoid sinus, subtentorial collection, paranasal sinus disease, and severe bilateral proptosis with periorbital soft tissue swelling. (Figure 2.) The patient was treated empirically with intravenous antibiotics and admitted for suspected septic cavernous sinus thrombosis with periorbital cellulitis.
Lateral canthotomy and cantholysis were performed after admission to relieve his elevated intraocular pressure, followed by an emergent orbital depression by total ethmoidectomy and sphenoid sinusotomy. The patient also suffered from meningitis and recurrent subdural empyemas, which required multiple subdural drains and neurosurgical interventions, including placement of a VP shunt for obstructive hydrocephalus. Cultures grew Streptococcus anginosis andStreptococcus viridins, and Propionibacterium, and antimicrobial therapy was titrated to penicillin G, which resulted in clinical improvement and infection clearance. The patient was discharged to a rehabilitation facility with complications, including blindness in the right eye and a permanent VP shunt.
Dural venous thrombosis is caused by thrombosis of a cerebral vein or occlusion of dural sinuses. (Medicine 1986;65:82; Arch Intern Med 2001;161:2671.) The cavernous sinus is the most frequent dural sinus to become thrombosed secondary to infection because of its irregular trabecular structure that allows bacterial trapping. (J Neurosurg 1976;45:169.) It is a rare disease with serious sequelae, including a 30 percent mortality rate, spread of infections such as meningitis and cerebral abscesses, persistent oculomotor weakness, blindness, hemiparesis, and pituitary insufficiency. (N Engl J Med1983;309:1149.) The prevalence of septic cavernous sinus thrombosis is most common among men (21% vs 10%), mainly because of a higher frequency of ear, nose, and throat infections in this population. (Stroke 2009;40:2356.)
Sinusitis, most commonly sphenoid and ethmoid infections, is a common nidus in infections that preclude cavernous sinus thrombosis. Facial infections drained by the ophthalmic vein and dental infections drained by the pterygoid venous plexus also put patients at risk for this complication. (Orbit 2006;25:39.) Sphenoid sinus infections typically spread contiguously through the lateral air sinus wall, while ethmoid sinus infections extend laterally to the orbital cavity with subsequent extension to the ophthalmic veins. (N Engl J Med 1983;309:1149.) The intricate structure of the cavernous sinuses creates a potential location for trapping, seeding, and proliferation of microorganisms. This results in thrombosis and stasis of dural venous return from the ophthalmic and cerebral veins. The venous status leads to increased capillary pressure with subsequent decreased cerebral perfusion, leakage into the interstitial parenchyma, and cytotoxic edema. (Neuroradiology 2002;44:481; Arch Neurol 2001;58:1569.)
Early signs and symptoms of cavernous sinus thrombosis are nonspecific, and they usually mimic primary headache syndromes. Headaches are the most common early sign, followed by fever, proptosis, chemosis, altered mental status, and cranial nerve III and VI palsies. Brain MRI is the most sensitive and specific imaging modality for cavernous sinus thrombosis, but head CT scan and lumbar puncture are useful to evaluate the emergent or unstable patient. Mainstay therapy is broad-spectrum antibiotics with meningitis dosing, along with anticoagulation, glucocorticoids, and surgical drainage. (Pediatr Crit Care Med 2004;5:86; J Laryngol Otol 2002;116:667.) Septic cavernous sinus thrombosis is relatively rare but the prognosis of patients is relatively poor. Many patients can initially present with nonspecific symptoms, with the most common mimicking primary headache syndromes. Therefore, it is important for the emergency medicine physician to consider septic cavernous sinus thrombosis patients presenting with headache, especially in patients with a history of chronic sinusitis.
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