A 23-year-old lady was admitted to the ICU with respiratory distress requiring emergent intubation on 25 March 2014. She was being managed on the ward for bilateral infected leg ulcers, on a background of systemic lupus erythematous (SLE), hypertension, rheumatic fever, chronic renal failure, microscopic haemolytic anaemia, and extensive oesophageal ulceration. Her admission weight was 60.5 kg.
The cause of her respiratory failure was invasive aspergillosis and CMV pneumonitis. This was further complicated by microangiopathic haemolytic anaemia and thrombocytopenia thrombotic purpura requiring plasmapheresis, liver dysfunction, and renal failure requiring continuous renal replacement therapy. A percutaneous tracheostomy was performed on day 10 of her ICU admission. By day 22, she had lost > 25% weight from admission despite provision of enteral nutritional support aimed at 120% of predicted caloric requirements. She was clinically severely deconditioned (serum albumin 22) with evidence of fat and muscle wasting, undergoing a protracted wean from the ventilator (on day 30 she was still receiving pressure support ventilation 12/5 and transitioned to T-piece ventilation trials on day 31), and globally weak with 1-2/5 power throughout.
She was commenced on testosterone (Sustanon®) 250 mg IM on day 32. Subjectively her appetite improved as did her ventilator weaning and she was decannulated 3 days after the first dose. After further consultation with the immunology team, the Sustanon was replaced by 200 mg danazol daily from day 43 due to improved safety in SLE. Upon discharge to the ward (day 46), her upper limb strength had improved to 3-4/5 bilaterally and 2/5 power in the lower limbs. She was able to move from supine to standing with minimal assistance and continued with tilt table for strengthening and stretching. After 3 weeks of rehabilitation on the ward, she could walk approximately 20 m unassisted with a frame. She was subsequently transferred to a rehabilitation unit on day 62 and discharged home on day 73, after 30 doses of danazol.


A 62-year-old male presented to the Emergency Department on 14 June 2015 with fevers and rigors, 5 days after a complex transoesophageal AF ablation (admission weight 139 kg). Following a brief cardiac arrest on the coronary care unit, a CT chest revealed an oesophageal perforation and atrio-oesophageal fistula. He underwent urgent repair of the left atrio-oesophageal fistula. Postoperatively he developed mediastinitis and vasopressor dependent shock. On day 8, he developed severe abdominal pain and had a right hemicolectomy and ileostomy for caecal perforation. Following these complications, he was severely deconditioned (critical illness myopathy was evident from day 9) and received a tracheostomy on day 16. Despite optimal nutritional supplementation, he was losing weight (at one point he lost 6 kg weight in one week, and from admission weight to time of administration he had lost 16.6% of admission weight) with evidence of fat and muscle wasting. Due to the profound weakness in all limbs, an electromyogram (EMG) was performed on day 39, which was consistent with severe critical illness myopathy and mild axonal degeneration neuropathy.
He was prescribed nandrolone 50 mg IMI on day 82. At this point, despite daily physiotherapy throughout his stay, he required full hoist transfers. At the time of his second injection (day 90) his strength was dramatically improving with 3-4/5 power throughout. Serial testosterone measurements decreased from 10 before first dose to 5.7 before the second dose and 7.3 before the third dose. Although he still required full hoist for transfers, he could perform up to 6 reps of sitting to standing with ArjoHoist®. He was also able to sit unassisted for 30 minutes. On day 95 he was transferred to a rehabilitation unit and received his third dose of nandrolone the following day. He eventually flew back to Queensland (his home) and received ongoing rehabilitation and strengthening at a local hospital.


A 49-year-old male was admitted on 7 April 2015 with worsening abdominal pain on a background of known diverticulitis and colovesical fistula. After an initial anterior resection and cystectomy, he returned to theatre a further 5 times due to anastomotic breakdown and faecal peritonitis. He also developed multiorgan failure as a result of septic shock.
During his ICU stay, he lost approximately 16 kg (17% of admission weight) over 2 months, despite adequate parenteral and enteral feeding. In addition, he had overwhelming critical illness weakness with severe limb weakness. On day 29 after admission, he required pressure support ventilation via his tracheostomy and had only a flicker of movement in his limbs distally. He was given 50 mg IMI of nandrolone. One week later prior to receiving his second dose, he no longer required ventilatory assistance, and his power was measured at 2/5 on the left side of his body and 2+ on the right. He received subsequent doses on days 36 and 48.
At day 46, he was sitting on the edge of the bed with assistance and on day 48 he could walk a few assisted steps with a frame. His tracheostomy was removed on day 51. He was discharged from ICU on the 2 June (54 days after admission) with muscle power measured at 4/5 bilaterally (3/5 ankle/toes). On discharge from hospital on day 85 he was able to independently move, including up and down a flight of stairs.


A 70-year-old male, with a background of colonic cancer resection (1997) and recurrent small bowel obstructions (SBO), was admitted on 10 July 2015 with another SBO. During this admission, his weight dropped to 42 kg (BMI 13.5 kg/m2) with evidence of severe fat and muscle wasting. The weight loss was attributed to severe malnutrition related to chronic poor oral intake. He was commenced on total parenteral nutrition (TPN) after failed enteral feeding. Dexamethasone and mirtazapine were trialled as appetite stimulants, but he developed further obstruction which was managed conservatively.
He was severely deconditioned and had not been able to move out of bed for the first 20 days of admission due to profound weakness. He was not receiving mechanical ventilation. He was severely fatigued on transfer to the commode or shower and had 3/5 power throughout his limbs. He was able to ambulate less than 10 m with a frame. Nandrolone 50 mg IMI was prescribed to assist predominantly with weight gain, but also with deconditioning. He received his first dose on day 60 and a subsequent dose on day 69. He gained 4.5 kg following his first dose and was able to ambulate independently for gradually increasing short distances with a frame. He was discharged on day 89 with home TPN and rehabilitation in the home.


A 57-year-old woman was admitted to hospital for ileus status and metabolic disturbance. She had a history of paranoid schizophrenia, thyroid gland hypofunction, and hypertensive disease. No records of positive heart auscultation finding were found. Her ECG 1 year before death showed signs of left ventricular hypertrophy; echocardiography was not performed. The patient died with symptoms of heart failure and was indicated for autopsy. At autopsy, the main findings were distended intestines with numerous skybala in the colon and pulmonary edema.


A 52-year-old woman came to the emergency department (ED) for hemodialysis (HD) due to end-stage renal disease (ESRD). She had spent the preceding several weeks in an outside hospital being treated for pneumonia and bacteremia with daptomycin. She subsequently left against medical advice (AMA) after having her dialysis access catheter removed. She presented to our ED because she needed HD vascular access placement and re-initiation of dialysis treatments. Her medical history included chronic kidney disease secondary to hypertensive nephrosclerosis, anemia, hypertension, deep venous thromboses (DVT), systemic lupus erythematosus, and a seizure disorder of unknown etiology.
The patient, a Jehovah’s Witness, refused blood transfusions; therefore, her anemia was being treated with intravenous (IV) administration of iron, epoetin alfa, and folate. Other medications included nifedipine, clonidine, metoprolol, sevelamer, and prednisone. She was allergic to amoxicillin, azithromycin, hydralazine, labetolol, linezolid, morphine, and vancomycin. She reported previous IV heroin use many years earlier and previous cigarette smoking. She denied alcohol use or any current drug or tobacco use.
Upon arrival, she was alert and in no acute distress with a fever of 38.3° Celsius, heart rate of 87 beats per minute (bpm), blood pressure of 110/65 millimeters mercury (mmHg), respiratory rate of 17 breaths per minute, and pulse oximetry of 99% while breathing room air. She weighed 80 kilograms and was 5 feet 6 inches tall. Her head was normocephalic and atraumatic with moist mucous membranes. Pupils were anicteric, equal, round, and reactive to light and accommodation. The neck was supple and without lymphadenopathy or tenderness. Her lungs had coarse breath sounds with mild bibasilar crackles but no wheezes or rhonchi. There were no retractions or increased work of breathing. Her heart was of regular rate and rhythm without murmurs, rubs, or gallops. Her abdomen was soft with normal bowel sounds and without distention, tenderness, rebound, or guarding. There was no costovertebral angle tenderness. The lower extremities had 1+ pitting edema, 2+ dorsalis pedis pulses, and were without tenderness or deformity. The patient had normal strength and muscle tone throughout all extremities with intact sensation. Old fistulas were present in the left and right upper extremities without palpable thrills. She was alert and oriented to person, place, and time.
The patient’s initial laboratory values are shown in . These were significant for a slight leukocytosis, anemia to 5.3 g/dL, thrombocytopenia, hyperkalemia, and an elevated creatinine of 11.9 mg/dL. Her initial electrocardiogram (ECG) showed a sinus tachycardia with T-wave inversions in leads I and V6 (). This was unchanged from a prior ECG. The patient was admitted to the medicine team and was started on daptomycin. While awaiting bed placement, a non-tunneled left femoral dialysis catheter was inserted by the medical intensive care unit (ICU) fellow for initiation of HD. Placement was confirmed by the easy drawback of blood from all ports. During the consent process for catheter placement, it was documented that the patient stated she “would rather die than receive blood transfusions.” Following catheter placement, an attempt was made to start HD, but she became hypotensive and complained of weakness almost immediately. Her vital signs during the initial HD attempt were a blood pressure of 85/56 mmHg with a heart rate of 105 bpm.
Because the patient was symptomatic and hypotensive during HD, continuous renal replacement therapy (CRRT) was initiated. Shortly afterward, she became hypotensive, unresponsive, and had a tonic clonic seizure. Vital signs at that time were a heart rate of 113 bpm, blood pressure 75/48 mmHg, respiratory rate of 20 breaths per minute, and oxygen saturation of 78% on room air. A brief, repeat physical exam showed the patient was unresponsive to painful stimuli and her pupils were equal and reactive. She was given 4 mg of lorazepam and intubated for airway protection. A right arterial femoral line and a right femoral triple lumen venous central line were placed. A chest radiograph confirmed endotracheal tube placement (). CRRT was halted but the patient remained in shock despite bolus infusions of crystalloid, so vasopressors were started. She was receiving escalating doses of vasopressors when repeat laboratory values indicated a hemoglobin of 1.6 g/dL ().
Shortly thereafter she went into cardiac arrest with a rhythm of pulseless electrical activity (PEA). Return of spontaneous circulation was achieved after six minutes of cardiopulmonary resuscitation. Increased abdominal distention was noted during the resuscitation; therefore, a pressure-sensing urinary catheter was introduced. Her peak airway and bladder pressures were measured at greater than 60 cmH2O and 50 mmHg, respectively. Surgery was then consulted. A massive transfusion protocol was initiated after her next of kin agreed to allow the transfusion of blood products. A focused assessment with sonography for trauma (FAST) was performed, showing free fluid in Morrison’s pouch. As resuscitative measures were continued, an additional study was obtained and a diagnosis was made.


A 74-year-old man on rivaroxaban for paroxysmal atrial fibrillation presented with the gradual onset of neck pain. The pain started while he was walking in the woods and was associated with progressive weakness and numbness from the clavicles downward. He was able to walk back to his cabin, but upon arrival he was unable to maintain his balance and fell forward striking his head. He denied any loss of consciousness. He was unable to move for about 45 minutes. Emergency medical services was called and they noted the patient to be completely paralyzed with fecal incontinence. He also had shortness of breath. During his transport to the emergency department (ED) he started to regain strength and feeling in his arms and legs and improvement of his shortness of breath. He denied any recent fevers, upper respiratory infection, rash or tick bites. All other review of systems was negative. Past medical history was significant for hypertension, atrial fibrillation, and coronary artery disease.
On initial examination, the patient was alert and oriented to person, place, and time. Temperature was 92.0 degrees Fahrenheit tympanic, pulse 56 beats per minute, respiratory rate 20 breaths per minute, blood pressure 122/56 mmHg, oxygen saturation 100% on four liters nasal cannula. Lungs were clear to auscultation bilaterally without wheezes, rhonchi, or rales. Heart was regular rate and rhythm, without any murmurs. Abdomen was soft, non-tender, non-distended with normal bowel sounds. Back had no evidence of trauma or deformity, non-tender to palpation. On extremity exam he had 4/5 strength in all extremities. After 20 minutes in the ED, he developed flaccid paralysis of all extremities with 0/5 strength. His voice also became softer and he developed shortness of breath. After five minutes he was able to wiggle his left toes. Over the next hour he slowly regained strength in his right lower extremity and his voice returned to normal. After another 40 minutes the patient was able to move his right upper and lower extremity and wiggle his toes on his left lower extremity. He was still unable to move his left upper extremity.
A computed tomography angiography (CTA) of the chest, abdomen, and pelvis was performed and did not show any evidence of aortic dissection. MRI of the cervical spine showed a prominent epidural hematoma, primarily dorsal, that extended from the foramen magnum down to cervical vertebra C7 and contributed to severe mass effect on the thecal sac (). Findings were the worst at C2–C3, where the hematoma measured 7–8 mm in width with compression of the cervical spinal cord and associated cord signal abnormality. In retrospect, findings were also visible on the preceding CTA. Patient was taken emergently to surgery for evacuation of the hematoma.


A 58-year-old African-American female with a history of traumatic brain injury presented to the emergency department (ED) from her nursing home after experiencing several episodes of coffee-ground emesis that started on the day of presentation. She was noted to have three additional episodes of coffee-ground emesis mixed with maroon-colored clots in the ED but did not appear to be in distress. Past surgical history included the placement of a 25 French (Fr) PEG tube approximately one year prior. The PEG had been replaced by a Foley catheter at some point, but there was no available associated documentation.
On physical examination, she was normotensive (133/83 millimeters of mercury), tachycardic (109 beats per minute), and tachypneic with mildly increased work of breathing. She was afebrile and her oxygen saturation was greater than 95%. Her abdomen was distended, firm, and tender to palpation throughout. She demonstrated some guarding with no rebound. Normal bowel sounds were present and no hepatosplenomegaly was noted. Rectal exam revealed brown stool that was guaiac negative. The feeding tube site was clean and without erythema, with a Foley catheter entering the site secured by fenestrated gauze.
The patient was resuscitated following institutional treatment guidelines for sepsis. Laboratory data were within normal parameters except for a lactic acid of 4.2 mmol/L. In addition, there was some concern the patient may have had gastrointestinal obstruction or perforation. The patient was taken for computed tomography (CT) of the abdomen and pelvis with intravenous (IV) contrast. Imaging revealed the Foley catheter traveling through the PEG tract with the balloon resting in the gastric antrum. The stomach was filled with fluid, the small bowel was unremarkable, and the colon was diffusely distended with air-fluid levels and no transition zone ( and ).
The Foley balloon was deflated, pulled back, and re-inflated. Following retraction of the Foley catheter, the patient did not experience any further episodes of emesis. The patient was admitted to the inpatient medicine service for urgent endoscopy and observation. The next day the patient underwent endoscopy during which the Foley catheter was replaced with a 20 Fr PEG tube. The lactic acidosis resolved with IV hydration, and no source of bleeding was identified.


A 61-year-old female with a history significant for polycystic ovarian syndrome complicated by splenic cysts status-post splenectomy and chronic lymphedema presented to the hospital with cellulitis involving both lower extremities. In the prior eight months, she had six episodes of cellulitis caused by group B Streptococcus involving her lower extremities. She was hospitalized, and blood cultures grew out group B Streptococcus. She received treatment with intravenous levofloxacin and vancomycin and demonstrated clinical improvement. However, careful inspection of the area of cellulitis on her lower extremities revealed papillary lesions consistent with a condition known as papillomatosis cutis lymphostatica (). For this condition, she was treated with compression stocking and amoxicillin 500 mg four times daily in the outpatient setting.


A 33-year-old male with uncontrolled HTN and end stage renal disease (ESRD) presented to the emergency department (ED) just prior to scheduled hemodialysis due to severe HTN. Initial blood pressure was 248/165 mmHg and the patient complained of a worsening headache and throbbing pain behind his eyes. He admitted to missing his last session of dialysis and his laboratory values were remarkable for a blood urea nitrogen (BUN) of 53mg/dL, creatinine (Cr) 4.67mg/dL, and serum bicarbonate (CO2) 21 mEq/L. Remaining serum electrolytes and hepatic function panel were normal. Symptoms were attributed to volume overload due to missed dialysis, and treatment with furosemide 40mg intravenous (IV) was initiated. Repeat blood pressure was 197/134 mmHg, and the patient was transported to the dialysis unit.
Upon completion of dialysis he remained hypertensive and immediately returned to the ED with severe headache, dizziness, and unilateral weakness. His blood pressure was 200/135 mmHg, heart rate 93 beats per minute, respiratory rate 22 respirations per minute, temperature 98.9°F. Physical examination was significant for pupils equal and reactive to light bilaterally with extra ocular movements intact, cranial nerves II–XII intact, [3/5] strength in the right upper extremity, [5/5] strength in left upper extremity, [2/5] strength in the right lower extremity, [5/5] strength in left lower extremity. Laboratory values showed the following abnormalities: BUN 39mg/dL, Cr 3.67 mg/dL, and brain natriuretic peptide 42500 pg/mL; serum electrolytes, hepatic function and troponin were normal.
Initial noncontrast head CT showed hypodense areas in the right lentiform nucleus and the medial bilateral occipital lobes concerning for acute to subacute infarct. Potential hypodense areas in the cerebellar hemispheres concerning for acute to subacute infarct could not be distinguished from artifact from adjacent bony structures. The patient’s unilateral right-sided weakness and CT findings brought stroke to the top of the differential diagnosis and the stroke team was consulted. The patient’s blood pressure was initially treated with one sublingual nitroglycerin prior to IV access, followed by 10mg intravenous labetalol. One hour after the patient’s arrival his blood pressure was 136/90 mmHg. The patient complained of continued headache and progressively worsening bilateral visual field deficits involving both inferior quadrants of each eye as well as bilateral loss of visual acuity. His blood pressure remained labile and he was subsequently placed on a nicardipine drip at 2.5mg/hr for more precise blood pressure titration.
Following blood pressure stabilization, an MRI brain without contrast (our institution’s stroke protocol) was obtained. MRI showed extensive T2 fluid-attenuated inversion recovery (FLAIR) hyperintensities involving the occipital lobe gray matter and the subcortical white matter of the occipital, parietal, and frontal lobes. T2 FLAIR hyperintensities were also present in the deep gray and white matter, periventricular white matter, cerebellum, midbrain, and pons. A mixture of cytotoxic and vasogenic edema was seen as diffusion-weighted hyperintensities involving the left body of the corpus callosum and an area of deep white matter in the posterior right frontal lobes ().
The patient was admitted to the stroke service and was eventually transitioned to oral anti-hypertensive medications. His vision began to improve 24 hours after admission and upon discharge eight days later he had markedly improved visual acuity: 20/20 in the right eye with a mild right inferior quadrantopia and 20/40 in the left eye. His hospital course was prolonged by dialysis requirements and transfer to the psychiatric floor due to suicidal ideation and depression stemming from his poor health and hospitalization.


A 66-year-old Bedouin woman with a past medical history of uncontrolled type 2 diabetes mellitus, dyslipidemia and hypertension presented to the emergency department (ED) with a chief complaint of abdominal pain for two days. She described the pain as sharp, constant, and located in the epigastric area radiating to her back. It was associated with nausea and vomiting. She denied any history of nonsteroidal anti-inflammatory drug or other analgesic use and had no known history of coronary artery disease or prior surgeries.
On presentation the patient appeared stable with normal vital signs. The physical exam was remarkable for a rigid abdomen with diffuse abdominal tenderness. An immediate acute abdominal series was non-diagnostic without evidence of pneumoperitoneum. Analysis of venous blood revealed significant metabolic acidosis (pH 7.29, HCO3− 15.6 mmol/L, pCO2 26.2 mmHg, lactate 4 mmol/L). Computed tomography (CT) of the abdomen and pelvis was subsequently performed, which demonstrated free intraperitoneal air suggestive of a perforated viscous (). After the CT, the patient began to experience new-onset chest pain. An electrocardiogram (ECG) was obtained showing ST-segment elevation in the inferior leads II, III and AvF ().
Given the concomitant presentation of two emergent pathologies, a multidisciplinary discussion was conducted between the emergency physician, cardiologist and general surgeon to determine the proper course of treatment. They unanimously agreed that cardiac catheterization and percutaneous coronary intervention (PCI) would take precedence over laparoscopic surgical repair of the patient’s perforated viscus. This decision was based on the clinical judgment that an acute STEMI was the more immediate threat to life compared to perforated viscus without evidence of active exsanguination. Consideration was also given to the rapid nature of PCI compared to laparoscopic surgery.
The patient received 80mg pantoprazole intravenously (IV) as a temporizing measure for suspected gastric perforation and was rushed to the catheterization laboratory. Prior to PCI she received 3000 units of heparin IV, 300mg of aspirin orally (PO) and 600mg of clopidogrel PO. Catheterization demonstrated significant coronary artery disease. The proximal right coronary artery (with right dominant anatomy) had near total occlusion of the artery (99%), consistent with thrombolysis in myocardial infarction (TIMI) grade 1 flow. Presence of a large coronary thrombus was seen, with minimal anterograde flow beyond the occlusion (). PCI with a bare metal stent (BMS) insertion was then performed successfully.
The patient was then transferred directly to the operating room (OR) in hemodynamically stable condition. She was sedated and intubated and laparoscopic surgery was initiated. A 2mm perforation was visualized in the prepyloric gastric antrum. The defect was repaired and an omental patch was placed. Operative time was less than 20 minutes. After the operative repair but while still in the OR, the patient became hemodynamically unstable with systolic blood pressure measuring 40mmHg. IV vasopressors were initiated and the patient was transferred to the ICU on a ventilator. She remained hemodynamically unstable 12 hours postoperatively despite resuscitative measures and maximal vasopressor support.
A repeat ECG was obtained, which again showed ST-segment elevation (). The patient was then taken for a second cardiac catheterization, which revealed a total occlusion of the right coronary artery due to early subacute stent thrombosis. The thrombus was partially evacuated but could not be completely removed. An additional BMS was inserted and the patient was transferred to the intensive coronary care unit where she continued to be hemodynamically unstable. The patient subsequently passed away an hour later.


A 30-year-old male with a past medical history of type 1 diabetes presented to our emergency department (ED) with three days of worsening diplopia, dysarthria, and dysphagia. The patient stated his initial symptoms included headache and blurred vision for which he was evaluated at an outside hospital and treated for a migraine headache. Thereafter, the headache resolved, but he noted progressive diplopia with the onset of dysphagia, dysarthria, and hoarseness. The morning of his presentation to our ED he complained of inability to swallow and had difficulty handling his secretions with progressive drooling. He also noted facial weakness and difficulty ambulating. Review of systems was significant for two children at home with upper respiratory illnesses. He was otherwise well prior to his presentation.
Vital signs in the ED were normal. His physical exam was significant for a well-appearing healthy male with pooling secretions and upright posturing requiring frequent suctioning of his oropharynx. Neurologically he had significant dysarthria and hoarseness, as well as bilateral and symmetric ptosis and opthalmoplegia (cranial nerve 3 and 6 palsies), with a weak gag reflex. He had symmetrically decreased 1/4 upper extremity reflexes and 2/4 lower extremity reflexes with ataxia on ambulation. His motor and sensory exams were otherwise normal. His labs were unremarkable including a white blood cell count, serum chemistry, liver function testing, and urinalysis. Bedside negative inspiratory force was −40 cm H2O (normal −80 to −100 cm H2O), and his vital capacity was 2.8 liters (normal 3 to 5 liters). The differential diagnosis at that time included concern for Guillain-Barré syndrome (GBS), specifically Miller-Fisher syndrome (MFS), as well as neuromuscular junction disorders such as myasthenia gravis, infiltrative central nervous system processes ( i.e.lymphoma, metastatic cancer), sarcoidosis, Lyme disease, botulism and tick paralysis.
Neurology was consulted with continued monitoring in the ED. Magnetic resonance imaging of his brain was unremarkable, as were the results of lumbar puncture. Extensive laboratory testing looking for infectious or autoimmune causes were negative, including human immunodeficiency virus testing, lyme disease titers, acetylcholine receptor antibody, and a ganglioside antibody panel. He was admitted to our step-down unit for close monitoring and empirically started on intravenous immunoglubulin for MFS while awaiting other studies. Early during his admission, it was disclosed to house staff that he was an IV drug user and shared needles with multiple persons. He had withheld this information because he did not want his family to know about his drug addiction. Given his worsening inability to handle oropharyngeal secretions, he was intubated and transferred to intensive care.
An electromyography (EMG) was performed during this interval showing decreased compound muscle action potential (CMAP) amplitudes, strongly suggesting the diagnosis of botulism. Both the state health department and Centers for Disease Control and Prevention (CDC) were contacted with an immediate request for botulinum anti-toxin. Confirmatory studies for botulism were sent and empiric penicillin G was given. Botulism antitoxin was received and administered with extubation the morning after administration. Ten days after his initial presentation he was discharged well and continued to improve on outpatient follow-up.


A 29-year-old male with a past medical history only significant for hypertension arrived to our emergency department (ED) with complaints of headache and dizziness. The patient stated that in the past he had experienced similar headaches of similar intensity; however, with this headache he experienced changes in vision, which was a new phenomenon. He described his headache as frontal and stated it started about three hours prior to arrival. Shortly after the onset of the headache he had approximately 30 minutes of blurry vision, numbness to left face, tongue and left arm. His wife also noticed slurred speech with deficits in hearing that also lasted approximately 30 minutes. The neurologic symptoms completely resolved by the time he arrived to the ED; however, his headache continued and he was experiencing worsening dizziness.
Upon arrival, his blood pressure was 151/88, pulse 80, pulse ox 99% and temperature of 97.9. Blood glucose was 132. Visual acuity was normal uncorrected. Electrocardiogram (EKG) showed normal sinus rhythm with normal intervals. Lab work obtained included a complete blood count, complete metabolic panel, and troponin I, which were found to be unremarkable. The only medication the patient was taking was lisinopril (10mg) for hypertension. He had an unremarkable physical exam. He endorsed a history of similar headaches, except for his complaint of subjective dizziness, and we found no neurologic deficits on our exam. Pupils were round and reactive to light. There was no peripheral vision deficit. Speech was clear. Cranial nerves II–XII were intact. Lungs were clear to auscultation bilaterally. Cardiac and abdominal exams were benign. Extremities had 5/5 strength bilaterally, 2/4 patellar reflexes and sensation was intact. Romberg test was negative. Recurrent headaches without prior neuroimaging and his reported neurologic phenomena prior to arrival prompted a non-contrast computed tomography (CT) of his brain in the ED. The CT revealed a 2.3 cm tumor versus mass versus CC in the third ventricle causing hydrocephalus (). Because of the patient’s presentation and the CT findings the decision was made to transfer him to a tertiary center with neurosurgery service available.
At the tertiary center the patient underwent magnetic resonance imaging of the brain with contrast that revealed a 1.2×1.7×2 cm lobulated mass at the anterior aspect of the third ventricle with mild hydrocephalus without mass defect. Patient was started on levetiracetam, labetalol, hydralazine and cefazolin sodium. On hospital day 2 he had an endoscopic resection of the mass through a frontal incision and an intraventricular shunt was placed. The mass was sent for pathology, which reported results consistent with a CC.
On postop day 1 a head CT was done secondary to patient complaining of continued headache. It demonstrated a moderate amount of intraventricular hemorrhage, pneumocephalus and subcutaneous gas seen along left prefrontal soft tissues (). All findings were thought to be secondary to surgery.
On postop day 3 the patient complained of headache with photophobia. Repeat head CT demonstrated mild residual ventriculomegaly with interval decrease in postop pneumocephalus and decrease in the intraventricular hemorrhage.
The patient continued to improve, had normal vitals and normal lab values and he was released home on postop day 6.


A 68-year-old male patient presented with a two-day history of a swollen, painless penis, fever (up to 38.7°C), and malodorous discharge from his preputial ring. His medical history included inguinal hernia repair five years ago. The patient denied any recent history of trauma, voiding symptoms, alcohol abuse, and diabetes mellitus or other systemic disease. He had no sexual intercourse during the last nine years, since his wife's death. Patient's children confirmed his history's information.
On admission, his temperature was 38.4°C and the vital signs were stable. Clinical examination revealed edema, tenderness, and diffuse crepitus along the penile shaft. The penile skin was dark-coloured, but there are no other abnormal findings. There was malodorous, thick, purulent discharge from his preputial ring and we could not retract the foreskin (). The scrotum, digital rectal, and inguinal lymph node examinations were normal.
White blood cell count was elevated (11.9 × 103/μL), hemoglobin value was within normal levels (11.2 g/dL), and C-reactive protein value was found to be highly elevated (182 mg/L with normal values < 3 mg/L). The other blood chemistry levels and urinalysis were in the normal range. HIV test and RPR test for syphilis were negative. Ultrasonography demonstrated a 3 cm hyperechogenic fluid collection with gas at the middle of the penile shaft, in contact with the right corpus cavernosum and corpus spongiosum. Moreover, there was gas in the right corpus cavernosum and hyperemia of the surrounding tissue (). The above-mentioned findings suggested the possibility of polymicrobial necrotizing infection.
Blood, urine, and pus cultures were obtained. Fluid resuscitation and antibiotic treatment with IV clindamycin, piperacillin-tazobactam, and vancomycin were administered, according to the Internal Medicine consultation.
The patient submitted to urgent surgical intervention under general anesthesia. Before the operation, a suprapubic tube and a 20-Fr Foley catheter were inserted. After circumcision and degloving of the penis, it was noticed that although glans appeared normal both cavernosal bodies were replaced by necrotic tissue and pus up to their middle. No blood clots were found but only partial expansion of the inflammation to corpus spongiosum and urethra. Both testicles were normal. Necrotic tissue was debrided to bleeding edges. Glans was still well-vascularised, despite ligation of dorsal arteries of the penis and of cavernosal arteries. However, partial penectomy was performed mainly due to the partial excision of corpus spongiosum and urethra (). Samples were collected for culture and histopathological examination.
Postoperatively, the patient remained afebrile. Pus culture suggested Enterococcus faecalis, Streptococcus gordonii, and Prevotella melaninogenica. Clindamycin was replaced by metronidazole according to the antibiotics' sensitivity diagram. Histology revealed acute and chronic inflammation and necrotic tissue. After repeated debridement and dressings twice a day, the penile stump improved at the 11th postoperative day. Penile skin flap was reapproximated over the surgical trauma's surface and the urethra was spatulated and approximated to the penile skin with sutures (). The patient was discharged on the 17th postoperative day. The Foley catheter was removed on the 20th postoperative day and the patient is able to void in standing position.


A previously healthy 35-year-old Hispanic man with a remote history of mild performance anxiety in late adolescence presented to our family medicine residency clinic to establish and seek care for acute onset of anxiety. The patient was a manager at a large manufacturing firm and had received a master’s degree. At the time of presentation, he was married with two children. He had no family history of mental illness and was not taking prescription medications. At his initial visit at the clinic, he reported that 9 days prior, he had taken one dose of “molly” while at a gathering with friends. The friend who had supplied the drug stated that it was “pure crystal MDMA.” According to the patient, this was his first lifetime use of MDMA. He had also consumed several alcoholic drinks that night, reportedly reaching the level of intoxication. He described having a “fine” experience with the drug and returned to his normal baseline for the next 2 days. On the third day after ingesting MDMA, he began to experience an increase in worry and agitation; he reported having panicked thoughts and development of palpitations, blurry vision, flushing, increased thirst, and insomnia. He stated that these symptoms increased over the coming days, prompting him to seek medical care. Regarding substance use history, the patient reported occasional social alcohol use since his early 20s, rarely to excess. He had used cannabis several times while in college (ages 18–22) and found that this precipitated anxiety and therefore he did not continue using it regularly. He denied any regular use of other illicit substances.
On the initial day that the patient met with a medical provider in the clinic, he reported a score of 20 (maximum score of 21) on the Generalized Anxiety Disorder 7-item scale [], an anxiety screening and rating tool commonly used in primary care offices. This score was consistent with a severe level of anxiety. The patient was prescribed buspirone, a serotonin 1A receptor (5-HT1A) receptor agonist, with a plan to uptitrate to 15 mg twice daily over the coming weeks. The patient was also referred to the clinic’s behavioral health service for adjunctive treatment and was promptly seen by a behavioral health consultant for their first session the following day. This initial visit involved an assessment of his biopsychosocial history and mood, a functional analysis of his anxiety symptoms, and a collaborative discussion regarding his treatment goals. Using interventions informed by cognitive behavioral therapy, the patient and the behavioral health consultant aimed to increase his coping skills and management of his anxiety symptoms and to improve his overall quality of life (e.g., reduce distress, increase enjoyment at home, and increase productivity at work).
The patient was seen for follow-up every 7–10 days by his PCP for the next month (see Table ). Simultaneously, he received behavioral health treatment each week following his first month of medical treatment in the family medicine clinic. He then established a therapeutic relationship with a counselor outside the clinic, where they reportedly engaged in talk therapy weekly. The patient reported only a slight improvement in his anxiety and panic symptoms despite the therapeutic dose buspirone; therefore, he was prescribed a selective serotonin reuptake inhibitor (SSRI) and a benzodiazepine and was referred to the psychiatry department for additional consultation. The consulting psychiatrist was concerned for MDMA-induced anxiety disorder and recommended discontinuation of buspirone and initiation of low-dose sertraline with slow uptitration. The patient benefited from behavioral health treatment specifically aimed at enhancing understanding and controlling the sympathetic nervous system (i.e., cognitive behavioral modeling, psychoeducation on the cycle of panic, and relaxation skill training). Behavioral health treatment was especially important as he awaited the clinical effect of his psychoactive medications.
Ongoing evaluation by the PCP, a consulting psychiatrist, and the behavioral health consultant supported a diagnosis of substance-induced anxiety disorder. He experienced persistent anxiety (reporting daily worry, panic, racing heart, dizziness, restlessness, and catastrophic thinking), and all of his symptoms developed shortly after ingesting a single dose of MDMA. His symptoms caused him significant distress and impairment in his employment as well as his family life. The patient denied clinically significant anxiety directly prior to taking MDMA; his only history of anxiety was performance anxiety many years prior. Therefore, he did not meet criteria for panic disorder or generalized anxiety disorder, because his symptom onset followed substance ingestion. Simultaneously, the patient reported transdiagnostic depressive symptoms, including hopelessness, fatigue, maladaptive thinking, and low mood. These symptoms, which also began following the patient’s use of MDMA, were etiologically attributed to his anxious physiological symptoms and thoughts, in particular the catastrophic and generalized worries that this one-time drug use had “ruined” his life. Consequently, his symptoms appeared to be explained by the substance-induced anxiety, as opposed to representing a discrete depressive disorder.
The patient initially tolerated the sertraline well and experienced a relatively rapid improvement in anxiety symptoms while taking 25 mg daily. After 8 days of the 25-mg dose, the dose was increased to 37.5 mg. After 2 days at this dose, the patient developed abrupt onset of suicidal ideation with a resurgence of anxiety and panic symptoms. Given the gravity of these new symptoms, the PCP and behavioral health consultant worked together and with the patient to devise a plan for ongoing care. He was able to see the behavioral health consultant for an urgent visit. The dose of sertraline was reduced to 25 mg, and plans were made for intensive outpatient mental health treatment at a nearby hospital.
While awaiting entrance into that program, his suicidal ideation and anxiety abated. As his symptoms improved, the behavioral health consultant supplemented sympathetic nervous system training with thought identification and cognitive retraining. These interventions served to address his reported catastrophic and demoralizing appraisals following the use of MDMA (e.g., “I am a terrible person for taking that Molly,” and “I have ruined my life forever”). He saw a second psychiatrist for additional recommendations. They concurred with the diagnosis of substance-induced anxiety disorder and the prescribed SSRI treatment. Eventually, the dose of sertraline was slowly increased to 50 mg with continued improvement in all symptoms and no further resurgence of suicidal ideation. The patient’s anxiety and panic were not well controlled until approximately 2.5 months after ingesting MDMA. At 6 months following his presentation, he was doing well with a plan to slowly taper the sertraline. He expressed gratitude for an interdisciplinary team approach and the unique benefits of skills training in tandem with psychopharmacological treatment.


A 61-year old female with diabetes mellitus and hypertension presented with a five-day history of epigastric pain and postprandial vomiting. A physical examination revealed a soft abdomen with mild epigastric tenderness. Labs were significant for an acute kidney injury. An abdominal CT scan following water-soluble hyperosmolar radiocontrast administration showed a 3.5 cm intraluminal calculus at the level of the third duodenal segment, diffuse pneumobilia, and an air-containing gallbladder, suggesting Bouveret’s syndrome (Figure ).
An initial improvement was noted later, followed by the recurrence of symptoms two days later. A repeat abdominal CT scan showed the migration of the duodenal stone and impaction at the distal jejunum with the dilation of the proximal loops, suggesting gallstone ileus (Figure ).
Subsequent jejunotomy and the successful extraction of the stone (Figure ) were performed, with no postoperative complications.


Peter and his family arrived to our clinical service when he was 14 months old. Perinatal anamnesis documented full-term birth after cesarean section with adequate extra-uterus adjustment, risk for insulin-dependent diabetes mellitus and reduced cranial diameters and good general health conditions at discharge from the Neonatal Intensive Care Unit (NICU). At 1 month, the analyses confirmed the significant reduction in brain volume. A diagnostic follow-up at 5 months documented the onset of epileptic seizures. Overall, Peter appeared to be easily dysregulated by moderate-to-high intensity stimulations and poor emotional regulation were reported.
To obtain more specific and fine-grained information on Peter’s emotional regulation during a standardized observational procedure.
During the Play episode, Peter was specifically sensitive to tactile (e.g., mother caressing) and auditory (e.g., mother singing) stimulations. In response to this kind of stimulations, Peter showed positive emotionality (e.g., rhythmic movements of the chest and arms together with wide mouth opening). During the Still-Face episode, Peter immediately appeared alert and sensitive to the suspension of maternal communication by exhibiting an immediate stress response (i.e., increase of motor activity and emergence of disorganized movements of the chest and arms). Interestingly, specific patterns of dyadic matching behaviors emerged including attempts to reach out with the arms directed to the mother’s body while simultaneously seeking eye-contact with her in order to be picked up. Such relational regulatory strategies were something that Peter usually did not show when distressed, as he easily became disorganized.
During the maternal unavailability episode Peter shows a clear ability to regulate his own behavior and emotions through relational strategies, something otherwise non-observable with a different observational procedure. Although such regulatory strategies may not be usual for the infant, it is clinically relevant to highlight that in response to specific relational and environmental adjustments (i.e., face-to-face interaction, lowered stimulation, enough time to organize other-directed attempts to self-regulate) Peter can access to more adaptive strategies to achieve regulation. This knowledge enriches the picture of Peter difficulties in self-stabilization and highlights a dyadic pattern to reinforce in order to support infant’s socio-emotional regulation.


Sarah was 8 months old when she first came to our clinical unit with her family. Sarah had a severe visual impairment. Moreover, Sarah’s mother reported that she faced many challenges in trying to understand her daughter and interacting with her in a reciprocal satisfying way. The visual impairment of the infant was a great barrier for the mother, who reported feelings of sadness and inadequacy as a caregiver.
To support the mother in detecting communicative intent and participation in Sarah’s behavior during the interaction and to increase the opportunity for the dyad to perceive more pleasure in their relationship.
We videotaped the FFSF paradigm with Sarah and her mother. During the Play episode, Sarah demonstrated to be able to orient her attention to auditory stimuli (e.g., maternal voice), but the mother rarely interpreted and responded properly to her orientation as communicative signals. The mother was frequently silent producing few attempts to engage with Sarah and remaining physically distant. The mother used the pacifier any time Sarah displayed minimal distress. The interaction appeared to be very difficult and – according to maternal reports – not very satisfying. During the Still-Face episode Sarah stood relatively quiet, with very few movements of the arms and legs. Nonetheless, a few seconds after the Still-Face episode onset she started to protrude in the direction of the mother, producing a lot more vocalizations compared to the Play episode and showing increased distress and negative emotionality. As soon as the Reunion episode started, the mother resumed to interact with Sarah and said: “Oh, you’re here then!” During the reunion phase the mother appeared more active in the interaction with her daughter and, after a period of negativity (i.e., 3040 s), Sarah displayed a smile toward her mother.
During the consultation the Sarah’s mother immediately said that she had never seen Sarah being so communicative and that the observation procedure “literally opened a new window in our relationship.” Looking at Sarah’s response to the Still-Face episode further allowed the mother and the psychologist to identify specific communicative behaviors which were previously undetected by the mother (e.g., active requests of being picked up, attentional focus on the mother, and sensitivity to maternal lack of communications). Moreover, the mother acknowledged that Sarah was indeed interested in interacting with her even in the presence of visual impairment. This increased acknowledgment of Sarah’s availability and desire to interact, and was also an opportunity to set up a collaborative consultation on specific modalities to reach out to Sara and to achieve better emotional closeness and reciprocal satisfaction.
This clinical vignette suggests that the joint observation of FFSF promote in the Sarah’s mother some changes in mental representation of her own infant. In turn, it reflects on subtle modifications in the maternal interactive style during interaction with Sarah.


A 70-year-old female was referred to breast re-implantation of the right side due to iatrogenic rupture and explantation during thoracic surgery. The patient had a medical history of cancer in the right breast in 1984 with subsequent treatment including unilateral mastectomy, radiochemotherapy and secondary reconstruction with a subpectoral silicone implant. In 2015 the patient was diagnosed with leiomyosarcoma in the right thigh and bilateral pulmonary metastases. The patient underwent video-assisted thoracoscopic surgery (VATS) wedge resection of the right lung and during this procedure iatrogenic perforation of the silicone implant and injury to the thoracic wall occurred. The thoracic cavity was closed and the perforated breast implant removed without diagnosis of the defect.
In stabile condition, the patient expressed a strong desire for breast re-implantation and during this procedure the defect of the thoracic wall and parietal pleura was observed. As the defect was minor, simple closure of soft tissue over the defect would be appropriate in patients not planned for breast reconstruction, however the patient in this case had expressed an extremely strong desire for breast reconstruction. In case of direct closure communication would persist between the lung and the capsular space and therefore it was necessary to close the defect with a thin layer of material allowing both secure closure of the defect and re-implantation. The highly vascularised capsule is known to be appropriate for creation of flaps and grafts, and has previously been used in management of issues in relation to breast implants []. The capsule tissue was an appropriate choice for creation of a pedicled flap in this case because the tissue presented a minimally invasive treatment option for the patient compared to closure with a muscle flap or addition of non-autologus tissue such ADM, increasing infection risk. The anterior part of the capsule in relation to the pectoral muscle was dissected free from the upper pole to the inframammary fold resulting in a medially and centrally vascularised flap. The flap was rotated with the agglutinating side facing downwards to cover the pleural defect and sutured shut. The flap was not expected to be airtight, however placement of the implant directly over the flap ensured necessary pressure to prevent displacement and air leaks. Pressure ventilation found the new capsular patch airtight. Next pleuracentesis was performed in order to control the pneumothorax and finally the flap was sutured in place to close the defect before placement of the silicone implant. Preventative iv. antibiotics were administered. Postoperatively the patient had discrete air effusion once the chest tube suction was discontinued and after five days chest x-ray showed a 5,2 cm apical lung pneumothorax. The patient had no pulmonary symptoms. At the one-week follow-up a regression of the pneumothorax from 5,2 cm to 3,1 cm was found and at the twelve month follow up the reconstruction was fully functioning and the patient asymptomatic.


A 45-year-old woman presented for a routine physical examination. Her pelvic ultrasound revealed a 4.2 cm left ovarian cyst. Initially, the lesion was managed conservatively with observation. Over the next 2 years, the patient remained free of symptoms; however, her ovarian cyst doubled in size measuring 8.1 cm by ultrasound. A laparoscopic left oophorectomy was ultimately performed.
Intraoperative pathologic evaluation revealed dark red cyst wall fragments, 7 cm in aggregate, and an unremarkable fallopian tube (Fig. ). The frozen section diagnosis was ovarian endometriosis (Fig. ), confirmed by evaluation of permanent sections. Among multiple additional permanent sections, several sections demonstrated atypical stratified epithelium in the subepithelial stroma within the cystic wall. The atypical cells had large, hyperchromatic nuclei, irregular nuclear contours, prominent nucleoli, scant cytoplasm, and numerous mitoses, consistent with malignant cells (Fig. ). The total size of malignant epithelium was approximately 15 mm. The remainder of the specimen was entirely submitted for microscopic examination and demonstrated ovarian tissue with endometriosis and an unremarkable fallopian tube. No evidence of teratoma was identified.
By immunohistochemistry (IHC), the malignant cells were diffusely positive for CK7, CK5/6, p63, and p16, and negative for CK20, WT1, GATA3, ER, and PR. p53 demonstrated wild-type staining pattern. Ki67 proliferation index was approximately 50%. (Fig. ).
Based on the morphologic features and immunohistochemical stain findings, the case was diagnosed as ovarian transitional cell carcinoma-like high-grade serous carcinoma. A differential diagnosis of metastatic urothelial carcinoma of the urinary tract was entertained; however, no lesions were identified in the urinary tract by ultrasound or computerized tomography (CT) scan. To rule out squamous cell carcinoma arising from teratoma, the entire specimen was examined. No evidence of teratoma was identified. The patient sought external pathology consultations from two large regional medical centers, both of which agreed with the original diagnosis.
Total hysterectomy and right salpingo-oophorectomy with pelvic lymph node dissection and omentectomy were performed. Grossly, the uterus, cervix, right ovary and fallopian tube were unremarkable (Fig. ). Microscopically, the right ovary, right fallopian tube, and other specimens revealed no evidence of malignancy. Interestingly, representative sections of the cervix revealed high-grade squamous intraepithelial lesion (HSIL). Eventually the cervix was entirely submitted for microscopic examination. Additional cervical sections demonstrated HSIL with focal superficially invasive squamous cell carcinoma. The depth of invasion was 4.0 mm and a horizontal extent was 6.0 mm involving only one of total 12 sections of the cervix. No lymphovascular invasion was identified. Examination of the right ovary revealed no evidence of teratoma. The FIGO tumor stage was IA2 (Fig. ). Prior to hysterectomy, testing for high-risk HPV was performed on the cervical cytology specimen by hybrid capture2 (HC2) method (Qiagen Inc., USA), and was positive (935 RLU; reference range: < 1.00RLU).
The original diagnosis of transitional cell carcinoma-like high-grade serous carcinoma was questioned. To correlate the findings in the ovary and cervix, DNA extraction was performed from the ovarian sections with carcinoma. The DNA extraction and purification was performed according to the manufacturer’s instructions using GenElute™ FFPE DNA Purification Kit (MilliporeSigma, Burlington, USA). Testing for high-risk HPV was performed by HC2 method was positive (141.3 RLU; reference range: < 1.00 RLU).
To further support the diagnosis of metastatic carcinoma, analysis of the patient’s peripheral blood for circulating tumor cells (CTC) was performed. Several malignant, triploid, CD45-negative epithelial cells were identified, suggestive of the presence of carcinoma cells in the peripheral blood (Fig. ).
The final diagnosis was metastatic cervical squamous cell carcinoma involving ovarian endometriosis.


A 52-year-old right-handed man with a history of idiopathic PD for 20 years presented with severe motor fluctuations including end-of-dose wearing off, freezing of gait, and peak-dose dyskinesia. He had a history of impulse-control disorders associated with dopamine agonists and a history of depression. After comprehensive multidisciplinary DBS assessment, he had undergone staged bilateral STN-DBS based on the ability to reduce dopaminergic medications with the target compared with the GPi. He underwent unilateral left STN-DBS placement (Activa SC DBS implanted with a 3389 Medtronic lead) followed by right STN-DBS 6 months later. Microelectrode recording was conducted sequentially, and typical STN-neuronal discharges were recorded. Kinesthetic cells were encountered and macrostimulation after final placement of the lead was unremarkable with non-specific side effects including dizziness at high levels followed by corticobulbar side effects with dysarthria. During initial DBS monopolar review 1 month after surgery, he noticed a sudden onset of “giddiness and euphoria” best described as a need to laugh that was overwhelming and precluded him from talking when activating right STN contact 0. The programming was done unilaterally and the contralateral DBS was off during the session. Symptoms appeared around 3.0 V [pulse width (PW) of 60 µs and frequency of 140 Hz] and became increasingly prominent as voltage was increased to 3.5 V. The patient reported a feeling of happiness and joy associated with involuntary laughing. Despite the jovial nature of his symptoms, he was uncomfortable and the sensation was not pleasant. He reported mild nausea and recurrence of euphoric, loose, and giddy feelings when activating adjacent contact 1 at 3.8 V. At 4.3 V, this feeling became persistent and more intense. Partial benefit in Parkinsonism was observed with ventral contacts and the patient developed right foot dyskinesia, mild reduction in bradykinesia, and reduction in rigidity around 3.5 V. The rest of his monopolar review was unremarkable with improvement in Parkinsonism with contacts 2 and 3 and dyskinesia at 2.5 V with contact 2. The uncontrollable laughter was reproducible after 6 months. Corticospinal side effects and non-specific dizziness were the most common side effects associated with stimulation of contacts 2 and 3. The final programming settings were bipolar with contact 3 positive, contact 2 negative, PW 90 µs, and frequency 140 Hz. His UPDRS-III score off medications at 1 year improved from 42 to 15 points.


Patient was a 39-year-old right-handed woman who received bilateral STN stimulation for progressive Parkinsonism. She reported progressing symptoms started 6 years ago with development of early motor fluctuations and dyskinesia. She underwent simultaneous placement of bilateral STN-DBS 5 years after her diagnosis of PD (Activa SC DBS, implanted with a 3389 Medtronic lead). While performing monopolar review 1 month post-operatively, she noted sudden and uncontrollable laughter when activating contact 0 at 2.0 V (PW of 60 µs and frequency of 140 Hz) on the left side. Her symptoms were intermittent, with sudden laughter at higher voltages and episodes of normal mood. Similarly, contralateral DBS was off during the programming session. Uncontrollable laughter was reproducible with unilateral left STN stimulation but did not occur with right STN stimulation. Programming other contacts provided improvement in parkinsonism without acute mood effects. The final programming settings were bipolar with contact 3 positive, contact 2 negative, amplitude 2.5 V, PW 60 µs, and frequency 140 Hz. Her UPDRS-III score off medications at 1 year improved from 51 to 26 points.


A 12-year-old boy presented to our clinic with a firm, nodular mass on the medial aspect of the right knee with a history of about 1 year. The lesion was not pruritic or painful, but mild tenderness was present. The patient stated that the size of the nodule had gradually increased over the last 3 months. Physical examination revealed a dark brown-black nodule, measuring about 1 × 1 cm, with two small nodular extensions from the periphery (Figs and ). There was neither ulceration nor crusting, and the dimple sign was negative. The patient gave no history of skin disease or other systemic disorders.
Dermoscopy revealed focally localized blue-red pigmentation areas on a white structureless background and pinkish red area at the periphery surrounded by brown pigmentation (Fig. ). The lesion was excised with 5-mm clear margins with preliminary diagnosis of nodular melanoma. On histopathological examination, a benign tumor composed of interlacing fascicles of spindle cells in the dermis with a storiform pattern and containing hemosiderin deposits was seen (Fig. A and B). Intracellular and extracellular hemosiderin deposits were demonstrated with the Prussian blue stain (Fig. C and D). Atypia and mitosis were not present. Factor XIIIa (FXIIIa) staining was positive, and CD34, S-100, smooth muscle actin (SMA), and cytokeratin (AEI/AEI3) stains were negative. The diagnosis of hemosiderotic DF was established with these histopathological findings. There was no recurrence during 1 year of follow- up.


A 46-year-old unmarried man was referred to the Department of Psychiatry, at Chosun University hospital by a local psychiatric clinic. Acute euphoric mood, labile affect, increased talkativeness, decreased need for sleep, and unrestrained buying sprees had developed about 3 weeks prior. Concurrently, he was convinced that he had sufficient money to start a global business, and was scheduled to meet the President of his country in secret. In addition, he experienced vivid visual hallucinations: he reported having recently seen hundreds of North Korean soldiers in the battlefield at dawn. He had already been prescribed psychotropic medications, including aripiprazole (5 mg/day) and alprazolam (0.5 mg/day), at a local psychiatric clinic 2 days prior. He was admitted to a psychiatric inpatient unit for further evaluation and treatment. Upon admission, the patient was found to have no personal or family history of psychiatric illnesses. He reported no sexual intercourse over the last 3 years. On mental status examination, he showed the characteristic psychopathology of psychotic mania, such as euphoric mood, grandiose delusions, flight of ideas, pressure of speech, and increased psychomotor activity. However, he did not show any impairment in concentration and immediate memory. His Mini-Mental State examination (MMSE) score was 29; he only failed to recall one item at delayed recall, reflecting unimpaired cognition. Further, no abnormalities were found upon physical and neurological examination. He was diagnosed with bipolar disorder with psychotic features. On the 1st day after admission, blonanserin, an atypical antipsychotic drug, was administered at a dose of 8 mg/day for alleviation of manic and psychotic symptoms.
On the 2nd day, routine blood test, including complete blood count, serum electrolyte, and biochemical tests, and chest X-ray, electrocardiography, electroencephalography, and brain magnetic resonance imaging (MRI) showed no aberrant findings. However, the patient showed a positive result for the serum venereal disease research laboratory (VDRL) test, at a titer of 1:32. Fluorescent treponemal antibody absorption test showed reactivity, whereas results of the HIV test were negative. On the 3rd day, analysis of cerebrospinal fluid through a lumbar puncture showed a positive VDRL result, at a titer of 1:8, and increased white blood cell count (22/mm3) and total protein (78.7 mg/dL). Since a positive VDRL result for the cerebrospinal fluid confirmed the diagnosis of neurosyphilis [], the patient was administered intravenous penicillin G, 20 million units daily, for 2 weeks. Along with intravenous penicillin G, an oral antipsychotic regimen (blonanserin, 8 mg/day) was maintained throughout the treatment period. From the 7th day onward, the manic and psychotic symptoms improved dramatically, which was supported by his report of gaining insight into illness and significant reduction of the scores of psychiatric symptom rating scales (Table ). By the time of discharge, on the 17th day, most psychiatric symptoms had disappeared. After 5 days of discharge, the patient visited our hospital, and neither mood symptoms nor psychotic symptoms were observed. He was administered a reduced dose of antipsychotic medication (blonanserin, 4 mg/day) for 2 weeks, which he later discontinued.


The patient is a 36-year-old right-handed female with a known history of VHL disease. Her 65-year-old father had been diagnosed with VHL disease and multiple cerebellar hemangioblastomas; her 39-year-old elder brother had also been diagnosed with type 1 VHL disease without pheochromocytoma because of a complete deletion of the VHL gene. This family pedigree is shown in .
At the age of 26, the patient underwent surgical treatment for cerebellar hemangioblastoma. She also had a spinal cord hemangioblastoma at 11th thoracic vertebra level, a renal cyst and multiple pancreatic cysts ().
When her father underwent surgical treatment for a cystic cerebellar hemangioblastoma at our hospital (International University of Health and Welfare Atami Hospital), she visited our hospital, at the age of 36, because of recently developed visual disturbance. Her visual acuity decreased gradually and her visual filed became narrow. The visual acuities at the first visit to our hospital were 0.1 on the right side and sensus luminis on the left side. The examination of her left ocular fundus showed a pale papilla ().
Magnetic resonance imaging (MRI) of the head showed a Gd-enhanced well-circumscribed mass on the left retrobulbar optic nerve in the orbital, and three-dimensional MRI showed the tumor enveloped the left optic nerve ().
The differential diagnoses for the tumor include optic glioma, optic sheath meningioma, optic nerve schwannoma and optic nerve hemangioblastoma. Among them, since the patient is a VHL patient, the most probable diagnosis was thought to be an optic nerve hemangioblastoma. Therefore, we made a decision to treat the tumor with stereotactic radiosurgery. At Shonan Fujisawa Tokushukai Hospital, the stereotactic radiosurgery was prescribed with the dose being 39 Gy/13 fractions using Novalis. The planning target volume was set at 0.7 mL, and D95 (95% of standard irradiation volume) was set at 35 Gy/13 fractions. The patient completely lost her vision after the radiosurgery. Eighteen months after the radiosurgery, the tumor volume slightly decreased (), but her vision has been still lost. The consent to publish the case has been given by the patient.


A 73-year-old man had a past operative history of ruptured colonic diverticulitis treated by Hartmann’s procedure in 2007, and perforated peptic ulcer treated by pyloroplasty in 2009. He suffered from abdominal and tarry stool for 5 days in March 2011, so he was admitted to a rural hospital for further survey and medication. An initial upper GI endoscopy showed gastric ulcer only, but hypotension with tachycardia and a drop in hemoglobin of 9 g/dl from 12 g/dl occurred the next day. Intravenous fluid and blood transfusion with packed red blood cell were prescribed. Abdominal aortic aneurysm (AAA) with rupture was highly suspected, so CTA of aorta (Fig. ) was carried out which disclosed an AAA with swollen bowel loop. He was transferred to our emergency department (ED) for consideration of vascular surgical intervention.
On arrival in our ED, vital signs were a respiratory rate of 16 breaths per min, a heart rate of 130 beats per min, a blood pressure of 98/73 mmHg, and a body temperature of 35.6 °C. Physical examination revealed a pale conjunctiva, no heart murmur, clear breathing sound, old operative scar over middle abdomen, and hypoactive bowel sound with tenderness over the periumbilical region. Leukocytosis, anemia, abnormal liver profiles, and metabolic acidosis were found. Laboratory investigations were summarized in Table .
A cardiovascular surgeon carried out emergent angiography of aorta, which depicted bleeding from the wall of the AAA and chronic total occlusion of the left external iliac artery, so a modified aorto-uni-iliac stent graft (Fig. ) was implanted with femoral-to-femoral bypass, which underwent smoothly. A general surgeon performed exploratory laparotomy and found a massive blood clot with a volume of about 1310 ml filling the entire lumen of the small intestine, a dilated and swollen duodenum about 6 cm in diameter with ecchymosis, and a fistula about 2x2cm over the third portion of the duodenum (Fig. ). Duodenostomy with primary closure for repair of fistula defect, partition of the duodenum between the 2nd and 3rd portions, and side-to-side gastrojejunostomy were completed smoothly. He was admitted to the surgical intensive care unit for postoperative care. CTA of aorta showed neither endoleakage nor intraabdominal abscess on postoperative day 17. He was discharged without complications and returned for follow up at the out-of-patient department on postoperative day 25.


A 2-year-old white boy who had no medical history presented to University Hospital Emergency Department with respiratory distress and fever. He is the second child of a Turkish father and a 40-year-old Uzbek mother; his older sister has no health issues. He was born at term weighing 3350 g. Milestones were reached at the appropriate age.
On admission to the primary hospital, he had jaundice and confusion; his blood tests showed anemia, thrombocytopenia, and liver and kidney dysfunction. Suspecting malignancy, abdomen and thorax computed tomography (CT) and cranial magnetic resonance imaging (MRI) were obtained, which revealed bilateral pleural effusions with more severe parenchymal compression on his left lung. Periportal edema and hepatomegaly were detected in the abdominal CT. The cranial MRI was normal. On the day of admission, he was transferred to our pediatric intensive care unit (ICU).
At the time of admission, a physical examination revealed a confused boy (Glasgow Coma Scale was 13) with a length in 90th percentile and weight in 90th percentile. He had generalized edema and icterus. His pulse rate was 132 beats per minute (bpm), respiratory rate was 45 breaths per minute, blood pressure was 120/54 mmHg, and temperature was 35 °C. Respiratory sounds were attenuated in his left lung. His abdomen was distended; his liver was palpable 4 to 5 cm below ribs. His Pediatric Risk of Mortality and Pediatric Logistic Organ Dysfunction scores were 20 and 11, respectively. Our preliminary diagnosis was multiple organ dysfunction secondary to sepsis. Antibiotic treatments were started with vancomycin (60 mg/kg per day) and meropenem (120 mg/kg per day) after sampling of pleural effusion, which showed characteristics of empyema (Table ). The cultures (urine, blood, catheter, and pleural fluid) were sterile. Due to increasing respiratory distress, he was intubated and artificially ventilated. A norepinephrine infusion was started to maintain cardiac output and prevent hypotension. HLH was diagnosed since he had elevated levels of serum ferritin, bicytopenia, splenomegaly, fever (> 38.5 °C), and hemophagocytosis shown in bone marrow sample, fulfilling five out of eight diagnostic criteria for acquired HLH. He had no urinary output for the last 72 hours; his blood urea nitrogen, uric acid, and creatinine levels were increased. Initial laboratory results are shown in Table . Therapeutic plasma exchange (TPE) and intravenously administered high-dose corticosteroid for HLH and continuous renal replacement treatment (CRRT) for acute renal failure were initiated.
Following 5-day high-dose corticosteroid administration, TPE, and CRRT, his clinical status and kidney and liver functions improved, and his vasoactive requirement and ferritin levels decreased. The norepinephrine infusion was decreased gradually and stopped after 4 days. He was extubated on the seventh day. On the tenth day of hospitalization he had a seizure; electroencephalography, MRI, and lumbar puncture did not reveal pathological findings. Since we excluded other pathologies that may cause seizures, he was thought to have septic encephalopathy. Antiepileptic medication was started, and he did not have a seizure in the follow-up period. CRRT was continued intermittently, and completely stopped on the 14th day of hospitalization. The antibiotic treatments were stopped on the 14th day of treatment. His immune functions were also investigated; his lymphocyte subset panel and immunoglobulin levels were found to be normal (Table ). The result of serologic testing for human immunodeficiency virus was negative.
Although his medical condition improved continuously, he had left spontaneous pneumothorax on the 21st day of admission as a complication of necrotizing pneumonia. Necrotizing pneumonia was diagnosed by thorax CT findings (Fig. ). Since pneumothorax persisted, left upper lobectomy surgery was performed on the 30th day of hospitalization. In the pathological examination of the excised lung tissue, features of CMV infection were observed and ganciclovir (10 mg/kg per day) treatment was started 2 days after surgery. In order to confirm the presence of CMV infection, CMV deoxyribonucleic acid (DNA) polymerase chain reaction (PCR), CMV DNA IgG avidity index, and CMV IgG and IgM tests were utilized. CMV IgM was found to be negative; however, CMV IgG was positive with high CMV DNA IgG avidity index (0.88; Table ). These results indicated that he had CMV reactivation, rather than an acute primary CMV infection. We determined the duration of ganciclovir treatment according to the level of CMV DNA PCR (10300 copies/mL) in the blood. Antiviral treatment was stopped after 17 days, when CMV DNA PCR results became negative. He fully recovered and was discharged from our hospital on the 50th day of admission. He had no health problem after discharge at 6-month follow-up at an out-patient clinic.


A 16-year-old male presented for evaluation of left shoulder pain, crepitus, and reduced ROM. Two weeks prior, he sustained a traumatic glenohumeral dislocation after a bicycle accident, which reduced spontaneously. Early rehabilitation provided no improvement to his restricted ROM or pain.
On physical examination, the patient appeared uncomfortable and extremely guarded. Apprehension and load and shift testing were consistent with anterior shoulder instability, and his ROM seemed reduced compared to typical dislocations. Plain film radiography revealed a 1 cm thin fragment of bone off the anterior glenoid, indicative of a bony Bankart (). Magnetic resonance imaging (MRI) confirmed this, but on critical examination of axial cuts, the fragment appeared flipped with subchondral bone superficial to articular cartilage (). Based on his pain and the redislocation rate of his age group after traumatic dislocations, surgery was recommended [].
Intraoperatively, a posterior portal was created using bony landmarks, after which anterior and high rotator interval portals were established with the assistance of spinal needle localization to achieve an appropriate trajectory onto the glenoid. A 30° arthroscope was placed in the high interval portal, adjacent to the biceps tendon, and was used for subsequent exploration of the joint and image capture. A thin bony fragment with the articular surface deep and the bony surface superficial was present (Figures and ). Both articular cartilage abrasion (), possibly from articulating with the exposed subchondral fragment, and a small Hill-Sachs lesion were present on the humeral head. The anterior portal was used to allow access for a liberator, grasper, and rasp which were used to free up the partially healed fragment, achieve reduction, and freshen bony edges. A transsubscapularis (TSS) portal, as described by Dwyer et al., was established using a percutaneous set (Arthrex, United States) and a small metal 5.4 mm cannula to minimize potential injury to the subscapularis muscle []. The fragment was fixed using a double row technique as described by Millet and Braun using three Arthrex PushLock 2.9 mm anchors (Arthrex, United States) and #2 FiberWire suture (Arthrex, United States) (Figures and ) []. The capsule was then advanced over the top of the fragment using three additional PushLock anchors ().
Postoperatively, the patient had no major complications. He followed a graduated-intensity 18-week institutional physical therapy program consisting of two three-week and two six-week phases, which included passive and active ROM exercises and strengthening of shoulder musculature (). Plain film imaging four months postoperative indicated anatomic reduction of the fragment (). On examination, active shoulder ROM was assessed for both the repaired shoulder and the contralateral shoulder. Compared with the contralateral shoulder, the repaired shoulder exhibited the same ROM but lacked 15° of external rotation with hands at sides and 15° with the arm at 90° abduction. The patient was seen again six months postoperative and on examination exhibited excellent strength and no instability symptoms but still lacked 15° of external rotation both with arms at the sides and at 90° of shoulder abduction. By this point in time, the patient had resumed sporting activities including cross-country skiing and track and field.


A 55-year-old woman with a noncontributory medical history was referred to the endodontic specialist clinic at Prince Sultan Military Medical City (PSMMC; Riyadh, Saudi Arabia) complaining of intraoral sinus with pus drainage in the right mandibular molar area. Clinical and radiographic examinations revealed a large amalgam restoration with recurrent caries and periapical and furcal radiolucency related to tooth #46. There was localized swelling in the gingival sulcus and the sinus in the gingival area. Tooth mobility was grade II. A midbuccal area with a narrow periodontal pocket > 10 mm was noted. The tooth had a negative response to the thermal vitality test (Endo-Ice; Hygenic Corp., Akron, OH, USA). The diagnosis was a necrotic pulp and chronic apical abscess.
Endodontic treatment was accomplished in two visits with calcium hydroxide [Ca(OH)2] medication between appointments. Local anesthesia (1.8 mL of lidocaine with epinephrine 1 : 100,000) was administered, and the tooth was isolated with a rubber dam. An access opening was created and four canals were located. During the second visit, the localized swelling and sinus opening were thoroughly resolved, and the root canal treatment was completed with RaCe NiTi rotary files (FKG Dentaire, La Chaux-de-Fonds, Switzerland) and 5.25% sodium hypochlorite irrigation. The tooth was obturated with lateral condensation of gutta-percha and AH Plus sealer (AH Plus; Dentsply Maillefer, Tulsa, OK, USA). No periodontal treatment was administered. Follow-up X-ray images were obtained from 1 year to 6 years, which showed complete healing of the bone in the periapical and furcation areas ().


A 30-year-old woman with a noncontributory medical history was referred to the endodontic specialist clinic at PSMMC complaining of pain and localized intraoral swelling in the left first mandibular molar. One year earlier, the tooth had undergone root canal treatment with cementation of the post and core and placement of a permanent crown. The clinical examination revealed localized swelling in the gingival sulcus. Periodontal probing through the furcation showed increased probing values with a grade II defect [] (). The radiographic examination revealed a large post in the distal canal and a large furcal lesion related to the distal root opposite the post placement. Iatrogenic root perforation was suspected.
After the administration of local anesthesia (1.8 mL of lidocaine with 1 : 100,000 epinephrine), the crown was removed with a crown removal instrument, and the post was removed with an ultrasonic instrument using a light brush and cutting motion to break up the cement around the post. A paper point was used to check for the presence of blood spots to determine the location and size of the perforation. The perforation site was irrigated with 2.5% sodium hypochlorite followed by drying of the canal and sealing of the perforation with mineral trioxide aggregate (MTA; Dentsply Tulsa Dental) mixed with saline and placed with a microapical placement system (Dentsply Tulsa Dental) and condensed with a paper point (). A wet cotton pellet was then placed on the MTA material. The tooth was temporized with glass-ionomer cement and cementation of the crown. At the second visit, the cotton pellet was removed and the MTA setting was checked.
The patient was referred to the prosthodontics department for permanent crown placement. Follow-up appointments at 3 months, 6 months, 9 months, and up to 4 years showed complete healing of the soft tissue and bone lesions and a normal pocket depth of 3 mm.


A 27-year-old woman with a noncontributory medical history was referred from the orthodontic department at PSMMC complaining of pus discharge from the gingival sulcus and slight gingival swelling on the palatal side opposite tooth #22 (i.e., maxillary left lateral incisor) after orthodontic treatment. Clinical and radiographic examinations revealed a sound tooth #22 with a mobility of grade II and a deep periodontal pocket > 10 mm mesial to tooth #22 with pus discharge from the pocket (). The thermal vitality test demonstrated a negative response. Moreover, the area was tender to percussion and palpation. Methylene blue stain was applied to exclude the presence of a crack or root fracture. It showed a negative result. The radiographic examination showed advanced bone resorption extending from the mesial bone crest toward the apex of tooth #22 ().
The diagnosis was necrotic pulp due to trauma during orthodontic treatment with symptomatic apical periodontitis. The first stage of the treatment plan was endodontic treatment, which was performed during two visits with calcium hydroxide medication between appointments (). Chemicomechanical debridement was administered with the ProFile.04 and ProFile.06 Taper Series 29 rotary instruments (Tulsa Dental Products) and sodium hypochlorite. The canal was obturated with lateral condensation of gutta-percha and AH Plus sealer (Dentsply Maillefer, Tulsa, OK, USA) (). The second stage of the treatment plan, which was a surgical procedure, was performed after the permanent composite restoration and a follow-up period of 3 months. Before surgery, the patient signed a consent form.
Local anesthesia (two 1.8 mL carpules of 2% lidocaine with 1 : 100,000 epinephrine) was then administered labially and palatally. A mucoperiosteal flap was raised mesially to the upper left canine tooth, and two vertical releasing incisions were formed in the anterior palatal area opposite teeth #21 and #23. A horizontal incision was formed from the left maxillary central incisor to the left maxillary canine. After flap reflection, a sling suture was placed in the tissue flap to secure it with the premolar tooth on the opposite side of the maxillary arch to aid the surgeon in improving visual and operative access by eliminating the need to manually retract the flap in the palatal area () []. Cortical bone was absent on the mesial side of tooth #22. The root surface was covered with black calculus and the area was obliterated with granulation tissues. After removing the granulation tissues and calculus from the root surface with ultrasonic tips (Figures and ), bone graft material (Puros Particulate Allograft; Zimmer Biomet Dental) mixed with saline was placed into the bony defect with a plastic instrument, and a resorbable barrier membrane (CopiOs membrane, Zimmer Biomet Dental) was placed above the bone graft. The flap was then repositioned and sutured with 4-0 Vicryl thread (Ethicon Inc., Somerville, NJ, USA). The patient was prescribed Augmentin (amoxicillin (875 mg) and clavulanic acid (125 mg)) (GlaxoSmithKline (Ireland) Ltd.) 1 g twice daily for 5 days and ibuprofen (600 mg) orally every 6 h for 2 days. Follow-up of the patient showed no tooth mobility, a reduced pocket depth of 4 mm, and healing of the soft and hard tissues ().


The second case is a 68-year-old female diagnosed with a cT4aN2cM0 laryngeal carcinoma located around the epiglottis. The interval with surgery was six and eight days for CT and MRI, respectively.
On the b800 diffusion-weighted image, a clear and homogeneous contrast with high diffusion restriction between tumor and surrounding tissue was visible. The ADC map shows corresponding low ADC values in the tumor and increased ADC values directly adjacent to the tumor. This was in correspondence with the T1-weighted MRI, which showed a homogeneous contrast uptake within the tumor and an increased uptake adjacent to the tumor. The T2-weighted MRI cranially showed an increased homogeneous signal compared with the surrounding tissue, whereas more caudally, the contrast between the tumor and the surrounding tissue was low.
In the images, a large ulcerative mass on the right side of the larynx was visible, probably originating from the laryngeal side of the aryepiglottic fold. The maximum diameter measured in the coronal plane is 4.6 cm. There is an extension around the right side of the epiglottis. Caudally, extension into the false and true vocal cord is found, while a subglottic extension is not observed. There is an obliteration of the paralaryngeal fat with a broad contact with the thyroid cartilage. The thyroid cartilage shows some signal enhancement but no invasion was visible. Anteriorly, an extension across the midline at the level of the false vocal cord is evident. Cranially to the thyroid cartilage on the right, some extension beyond the larynx without invasion of the strap muscles was present. In addition, the tumor extended minimally through the laryngeal incisura. No tumor invasion of the arytenoid or cricoid cartilage was apparent. The clinical tumor staging was T4. The patient was offered a total laryngectomy.
On histopathology, a poorly differentiated supraglottic squamous cell carcinoma of the basaloid type was visible. The growth pattern was mainly cohesive, with a diameter of 3.6 cm and bilateral extension. The tumor extended between the hyoid and the ventral part of the thyroid cartilage. The hyoid cartilage was slightly invaded by the tumor, resulting in a pathological T4 stage.
The volume of this tumor measured on histopathology was 10.9 ml, which was largely overestimated by GTVclinical with a volume of 21.6 ml, and comparable to the GTVDWI of 11.5 ml (Figure ). The clinical delineation showed more overestimation than the DWI segmentation (37% and 70% of the GTVclinical and GTVDWI-contained tumor, respectively), while a comparable region of the tumor was included in both GTV delineations (72% and 74% for GTVclinical and GTVDWI, respectively). The underestimation of the tumor extent by the GTVclinical was 2.1 mm and for the GTVDWI, it was 2.7 mm (Figure ).


The third case is a 68-year-old male with a cT4aN0M0 laryngeal tumor. The time interval between imaging and TLE is one and four days for CT and MRI, respectively. On the imaging, an enhancing mass with restricted diffusion was visible on the left true vocal cord.
In this patient, the tumor on DWI showed a poor heterogeneous patch-like contrast. Therefore, the automatic segmentation of the tumor was difficult and evaluated as not reliable. Also on T2-weighted MRI and T1-weighted MRI after gadolinium administration, the tumor was heterogeneous but more distinct from normal tissue. The tumor extended into the paralaryngeal fat with a broad interface with the thyroid cartilage. The adjacent thyroid cartilage showed edema and enhancement, which is suggestive of cartilage invasion. In addition, the cricoid cartilage was eroded on the left side. Caudally, there was an extension in the subglottis, 1.2 cm below the level of the laryngeal ventricle. An extralaryngeal extension was not observed and there were reactive edema and enhancement around the tumor.
On histopathology, a squamous cell carcinoma with an extension over the midline was visible, with a maximum diameter of 3.5 mm, predominantly cohesively growing. An extralaryngeal extension was observed at the dorsal and dorsolateral sides of the resection plane. Furthermore, focal perineural growth was observed. Erosion of the thyroid cartilage was not observed, while there was cartilage invasion in the cricoid (Figure ). The tumor was histopathologically confirmed as stage T4.
The delineated volumes of tumorHE, GTVclinical, and GTVDWI, respectively, were 7.9 ml, 13.5 ml, and 7.1 ml. The conformity of both delineations with the tumorHE was 48% and 19% for the GTVclinical and the GTVDWI, respectively. The percentage of the tumorHE included in the GTVclinical and the GTVDWI was 89% and 31%. The extent of the tumor was overestimated by both GTVs as 51% and 34% of the GTVclinical and GTVDWI-contained tumor, respectively. In contrast, the microscopic tumor extent was underestimated in other regions, as the tumorHE extended 1.5 mm from the GTVclinical and 11.3 mm from the GTVDWI (Figure ).


An 89-year-old man presented to the emergency department (ED) with a history of fever, nonproductive cough and exertional shortness of breath for a few days. He was started 4 weeks previously on intravenous daptomycin for 6 weeks for coagulase-negative staphylococcal bacteremia and infective endocarditis of mitral valve following a urinary procedure. Daptomycin was chosen in this patient for once daily dosing. He was a nonsmoker with no history of chronic obstructive pulmonary disease or asthma. In the ED, he was afebrile (temperature 99.8°F) with a heart rate of 77 bpm, blood pressure of 129/74 mm Hg and respiratory rate of 29 breaths per minute. His initial oxygen saturation was 72% on room air and required high flow oxygen to maintain his oxygen saturation. Chest examination revealed vesicular breath sounds with diffuse rales. Cardiac auscultation was normal. The rest of the physical examination was unremarkable.
Pertinent labs included white count of 7900/µl with peripheral eosinophilia of 6% (reference range: 0.0–6.0%), Eosinophil count 500/µl (reference range: 150–300/uL), C-reactive protein 27.95 mg/dL (reference range: <1.00 mg/dL), erythrocyte sedimentation rate 54 mm/h (reference range: 0–15 mm/h) and brain natriuretic peptide 102 pg/mL (reference range: 0–100 pg/mL). Electrocardiogram was unremarkable. Chest X-ray demonstrated hazy bilateral airspace opacification predominantly in the lower lobes. Computerized tomography (CT) scan of the chest revealed bilateral lower lobe ground-glass opacification with interlobular septal thickening (). Streptococcus pneumoniae and Legionella urinary antigens were negative. ANA, Rheumatoid factor, ANCA and respiratory pathogen panel were negative. Patient lives in Pennsylvania and denied travel outside the USA. Stool ova and parasites done were negative. Urine drug screen was not done but patient denied substance abuse. He was not on any over the counter pain medications. Blood and urine cultures done during hospital stay were negative.
With concern for DAEP, daptomycin was discontinued. Intravenous methylprednisolone at 60 mg every 6 h was started. Daptomycin was switched to intravenous vancomycin to complete the 6-week antibiotic course for infective endocarditis. He was also started on intravenous cefepime and metronidazole (2-week course) for broad-spectrum coverage of pneumonia. Resolution of eosinophilia (0.8%) with the appearance of neutrophilic leucocytosis (92.3% neutrophils with WBC of 12,500/µl) were noted. With improvement of his respiratory status, his methylprednisolone was stopped, and he was started on prednisone taper for 6 weeks. He was also started on prophylactic sulfamethoxazole-trimethoprim 800/160 mg two times daily until his prednisone would drop down to 20 mg daily. High flow oxygen was weaned off to nasal cannula oxygen.
Repeat CT chest () 2 weeks later revealed partial clearing of the diffuse ground-glass opacities. His respiratory status had improved, and he was maintaining saturation in low 90s on 2–3-L oxygen via nasal cannula. He was discharged home on prednisone taper, prophylactic sulfamethoxazole-trimethoprim, and supplemental oxygen. Unfortunately, he was lost to follow-up.


A previously healthy 21-year-old female patient born out of a non-consanguineous marriage presented at the emergency department of the Osmania General Hospital in India complaining vomiting and loose motion of unknown origin for five days. On physical examination, she had no other systemic abnormalities and she was admitted for further tests. During the stay, she gradually developed a petechial rash over both lower limbs and her platelet count was slightly lower than the normal range at 130,000 per microliter of blood. Vomiting and diarrhea subsided and she eventually developed a yellowish discoloration of the sclera and her urine turned dark yellow. Her total and direct bilirubin was 12.58 mg/dL and 9.8 mg/dL, respectively. Physical examination at that point showed that her liver was palpable at 3 cm below the costal margin and splenomegaly was also noted.
Further laboratory testing showed that her percentage of RBCs was low (3.8 million cells/ul), mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH) were normal at 98 fL/red cell and 30 picograms/cell respectively, while her mean corpuscular hemoglobin concentration (MCHC) was slightly in the lower range at 32 g/dL. Peripheral blood smear showed no spherocytes. Microcytes were present and hypochromic cells were also found. Osmotic fragility test showed normal osmotic fragility, while she also tested negative for Glucose 6 phosphate dehydrogenase deficiency. Hemoglobin electrophoresis was normal and the patient had a negative direct Coomb’s test and Sickling test. Ultrasound of the abdomen confirmed hepatosplenomegaly. A pedigree diagram was made (Figure ) and it showed that her mother and maternal aunt had similar symptoms but were never diagnosed for the condition. Due to the lack of appropriate laboratory facilities, the enzyme levels were not tested and the physicians relied more on the clinical presentation, physical examination and other laboratory results to make a clinical diagnosis of congenital non-spherocytic hemolytic anemia. She was treated for anemia (hemoglobin level of 6.7 g/dL) with blood transfusions and additional symptomatic care such as proper hydration was initiated. The patient gradually improved over a week and was discharged.


A 75-year-old man with a history of diabetes mellitus type 2, hypertension, and dyslipidemia presented to a local community hospital with neck and back pain that had persisted for 4 days. During a medical examination, he felt the abrupt onset of weakness in the upper and lower extremities and suddenly became unable to walk. Computed tomography (CT) of the brain did not reveal any abnormalities and the patient was transferred to our facility for further workup of the sudden quadriplegia. His vital signs upon arrival at the emergency room were as follows: body temperature, 35.9°C; pulse rate, 64 beats per minute; respiratory rate, 21 breaths per minute; blood pressure, 187/87 mm Hg; and oxygen saturation, 97% on ambient air. His speech, cognition, and cranial nerve function were normal. Manual muscle tests (MMTs) showed left-right symmetrical findings (Table ). The passive range of motion in all extremities was complete without pain or spasticity. Reflexes were bilaterally overactive in the biceps, triceps, and brachioradialis, especially in the patellar and Achilles tendons, and Babinski sign was also present bilaterally. A rectal examination revealed normal function. Proprioception (body position in space and vibratory sense) was preserved, but pain sensation was lost below the T4 level on the right side. Urinary incontinence also developed and a urethral catheter was inserted. Other than mild calcification of the aorta, whole-body CT findings including the cervical, thoracic, and lumbar spine were normal. Initial MRI revealed abnormal T2 signals in the cervical spine from C4 to C5 with cord compression from C3 to C7 (Fig. ). An orthopedic surgeon was consulted under consideration of a diagnosis of cervical spondylotic myelopathy (CSM). Repeat MMT findings showed a left-right asymmetrical change (Table ). The findings of cerebrospinal fluid (CSF) obtained via lumbar puncture on the day after admission were: white blood cells, 2 cells/mm3; red blood cells, 25 cells/mm3; total protein, 104.7 (normal 15–45) mg/dL; and glucose, 83 (normal (70–110) mg/dL. Hematological and biochemical findings were mostly within normal ranges except for mildly elevated creatinine, 1.24 mg/dL; blood sugar, 181 mg/dL; triglyceride, 173 mg/dL; and hemoglobin A1c, 6.4%. Antihuman T-lymphotropic virus type I (HTLV-I) antibody was positive in both blood and CSF specimens. No specific treatment except rehabilitation was performed until neurology consult because etiology was unknown. Diffusion-weighted contrast MRI (DWI) on hospital day 8 after a neurology consult revealed hyperintense signals predominantly at the grey matter, and a contrast T2 signal abnormality with a decreased apparent diffusion coefficient (ADC) (Fig. ). We started the patient on steroid pulse therapy because myelitis could not be completely ruled out, but this did not improve the neurological deficits. SCI was finally diagnosed as an exclusion diagnosis. The MRI findings on hospital day 20 were the same as the initial findings (Fig. ). The patient started to gradually recover even before the administration of steroid pulse therapy, although he needed a walking aid. He was transferred to a rehabilitation facility on hospital day 40.