A 60-year-old Pakistani male of Caucasoid origin was admitted to the dermatology unit with the following history. He had been operated for cataract 05 days ago. Post-operatively Co-trimoxazole tablets were given. Forty eight hours after taking the tablets the patient developed a severe burning sensation all over the body. This was followed by peeling of sheets of skin over the back, buttocks, thighs and neck. He had had a similar reaction to tetracyclines 12 years ago.
Initial examination revealed an asthenic, sick looking man with a B.P. of 130/90 mmHg, temperature 99 degree Fahrenheit and pulse 110/min. Hydration was poor. He was in obvious distress but conscious and oriented. On dermatological examination 40% of body surface area showed peeling of skin in sheets of more than 3 cm leaving behind superficial erosions. The back, buttocks, thighs and anterior aspect of the neck were primarily involved (). Skin tenderness and Nickolsky’s sign were positive. The mucosae were not involved.
At the time of admission the bio-chemical profile was urea 9 mmol/lit, creatinine 274 umol/lit, potassium 3.6 mmol/lit, and sodium 137 mmol/lit. The serum total proteins were 4.9 mg/dl with an albumin level of 3.4 mg/dl and an albumin/globulin ratio of 1.5/1. The blood counts, urinalysis, electrocardiogram and chest roentogram were unremarkable. Skin biopsy showed a sub-epidermal split with necrosis of the epidermis and eosinophilic infiltration.
On the basis of body surface area involved a fluid requirement of 4 lit/24 hours was deduced, half of which was administered as Ringer’s lactate and the other half as glucose saline. He was also put on intravenous Ceftriaxone 1 gm twice daily. The urinary out-put improved and temperature returned to normal. Blood chemistry repeated on the 3rd day revealed no abnormality. The very next day the patient developed multiple purpuric and ecchymotic spots over both thighs. Urgent investigations revealed raised fibrinogen degradation products levels in both urine and blood; however the serum fibrinogen, platelets and bleeding profile were normal. A diagnosis of compensated disseminated intravascular coagulation was made and fresh frozen plasma transfused. Over the next couple of days the skin lesions subsided and fibrinogen degradation products levels returned to normal. Subsequently the patient made an uneventful recovery and all the lesions healed without scarring.


A 45-year-old Pakistani female of Caucasoid origin was admitted to the dermatology ward with extensive peeling of skin over the back and buttocks. She had taken a quinolone (moxifloxacin) for fever 05 days ago which was followed by a morbilliform eruption and widespread peeling of skin. She was a known diabetic for the past 10 years on insulin injections. On examination she was conscious but distressed, dehydrated and febrile with a temperature of 101 degree Fahrenheit, B.P. 130/90, pulse 98/min. She had skin peeling involving about 60% of the body surface area including the back, buttocks, face, neck and limbs (-). Oral and conjunctival mucosae were severely involved ( and ) and Nicholsky’s sign and skin tenderness were positive. Biochemical profile revealed raised serum urea 10.7 mmol/lit, creatinine 75 umol/lit, sodium 137 mmol/lit, potassium 3.8 mmol/lit, her ALT was also raised 87 IU but serum bilirubin and alkaline phosphatase were within normal limits. The blood counts, urinalysis, X-rays chest and electrocardiogram revealed no abnormality. Skin biopsy showed sub-epidermal clefting with a mixed infiltrate of polymorphs. The patient was treated with intravenous dexamethasone 3 mg 8 hourly and intravenous ceftriaxone 1 gm twice daily, intravenous insulin on a sliding scale along with topical antiseptic dressings and fluid and electrolyte replacement therapy. The steroids were gradually tapered off and the patient exhibited an uneventful recovery over the next 2 weeks; all the skin lesions healed without scarring and there were no sequelae except for a corneal opacity in the right eye.


An 18-year-old African-American male with type 1 diabetes mellitus presented to the emergency department with a one-day history of lethargy and vomiting. Clinical examination revealed a dehydrated male with heart rate of 120 beats/min and a blood pressure of 136/66 mmHg. He was tachypneic with a respiratory rate of 35/minute; the pattern was characteristic of Kussmaul’s respiration. There was subcutaneous emphysema in both supraclavicular areas. Auscultation of the chest revealed a crunching noise over the cardiac apex and the left sternal border, synchronous with each cardiac beat (Hamman’s sign). Laboratory investigation revealed a metabolic acidosis with venous blood pH 7.08. Plasma glucose was 1438 mg/dl and bicarbonate < 5 mmol/l; ketones were present in the urine. Chest X-ray showed subcutaneous emphysema as well as pneumomediastinum (), confirmed by chest computed tomography (CT) ().The subcutaneous emphysema and pneumomediastinum resolved spontaneously within 72 hours of the initiation of treatment for diabetic ketoacidosis (DKA).


A 26-year-old Caucasian female presented in the emergency room complaining of a two-week history of right flank pain. Her past medical history was unremarkable but included an episode of pyelonephritis two years ago. Physical examination was unremarkable: normal pulmonary examination, heart murmurs S1, S2 +0 bruits, neurologic examination normal - negative focal signs, GI examination normal, tender non sensitive abdomen, normal bowel sounds, except for tenderness at the right costophrenic angle. Routine laboratory tests were within normal limits. Blood panel was normal, biochemical panel showed normal electrolytes and renal function, liver enzymes and amylase were within the normals. Urinalysis showed no significant findings and the urine culture was sterile.
The patient underwent abdomen ultrasound which revealed moderate pelvicalyceal dilatation in the right kidney and proximal ureter with no apparent cause. The kidney-ureter-bladder X-ray did not reveal abnormal findings (Panel A). However, intravenous pyelography showed a right hydronephrosis which had a characteristic fish- hook (reversed “J”) shape of ureter (Panel B, arrow). In addition, there was medial deviation of the ureter. No renal tract calcification was noticed. The findings were consistent with that of a retrocaval ureter [,], which was confirmed by computed tomography (CT) [].
The patient is currently followed in renal clinic and a surgical correction would be performed in the near future.


A 44-year-old Polish Caucasian male, farmer, was admitted to hospital due to 3-month history of high-grade fevers, loss of weight, diarrhoea and joint pain. Physical examination revealed swollen and reddened major joints of upper and lower extremities. Laboratory and imaging examinations excluded rheumatoid arthritis, ulceration and neoplasm. Upper endoscopy revealed non-specific inflammation of duodenum. Biopsy stains were not contributory. In view of signs and symptoms a strong suspicion of Crohn’s disease was made and the patient was commenced on prednisone 30 mg per day with a good result.
Several months later diarrhoea relapsed, malaise and loss of weight was noticeable. Laboratory tests were unremarkable (including creatinine level) except for hemoglobin which was below reference value (10 g/dL). Upper endoscopy was repeated and duodenum biopsy samples were collected. Histochemical stains showed periodic acid-Schiff (PAS)-positive particles in mucosa, which led to a diagnosis of Whipple disease. Trimetoprime-sulfametoxasole in dose of 960 mg twice per day was introduced. The patient was recommended to continue the treatment for at least one year. At that time diarrhoea subsided, test for proteinuria was negative and all other renal parameters were within normal limits.
One and half year later the patient was readmitted to the hospital due to lower limbs oedema, weakness and anorexia. Laboratory tests revealed nephritic proteinuria (4-6 g/day), increased concentration of creatinine (1.2 mg/dL) and erythrocyte sedimentation rate (115 mm), iron deficiency anemia, decreased glomerular filtration rate (GFR) (52 ml/min) and normal urea (42 mg/dL). A kidney biopsy was performed which showed secondary amyloidosis (). Computed tomography scans revealed enlargement of mesenteric and retroperitoneal lymph nodes with high amount of lipids which was suggestive of Whipple disease.
The patient received 1000 mg of cyclophosphamide, 20 mg of prednisone, and trimetoprime-sulfametoxasole. A month later he received second pulse of cyclophosphamide in dose of 400 mg. At this stage, creatinine concentration was 2.7 mg/dL and urea 170 mg/dL. Within next 3 weeks renal parameters markedly deteriorated and renal replacement therapy was started.
Three months later the patient was hospitalized again due to bloody diarrhoea, bilious vomiting, progressive malnutrition, anemia requiring erythrocyte transfusion and intradialysis hypotension. He denied having fever, abdominal pain or rectal tenesmus. On admission the patient was in poor general condition with orthostatic hypotension of 60/0 mm Hg and blood pressure of 80/50 mm Hg in recumbency. Heart rate was 64/min, body temperature was 36.6°C, BMI was 20. Muscular atrophy and malnutrition were easily seen. At this stage the results of basic laboratory tests were as follows: hemoglobin level 8.5 g/dL, hematocrit 25%, red blood cells counts 2.8 × 106/µL, white blood cells counts 5.67 × 103/µL, lymphocyte counts 16%, serum total protein 3.1 g/dL, albumin 1.6 g/dL, CRP 43 mg/dL and ferritin 1839 ng/mL. Additional biochemical tests revealed CD8 deficiency and abnormal CD4/CD8 ratio, decreased concentration of IgA, IgM and IgG, elevated level of IgE, reduced concentration of FT3 and testosterone, normal value of TSH, cortisol, prolactin and fasting insulin. Urine analysis detected proteinuria of 2.9 g/dL.
Upper endoscopy was performed, which showed sever inflammation of post-bulbar duodenum with diffuse fibrinous erosions. Endoscopic examination also revealed fistula 60 cm from incisors. Histologic staining of collected biopsy samples revealed blood extravasation with large number of PAS-positive macrophages (). This pathomorphologic picture was suggestive of Whipple disease. Subsequently, gastrointestinal series were performed which did not confirm the presence of fistula.
On the basis of above findings a diagnosis of severe exacerbation of Whipple disease was established. The patient was started on ceftriaxone (1 × 2.0 g per day) and total parenteral nutrition. Within few days of treatment diarrhoea and hypotension subsided. Repeated gastroscopy showed tremendous improvement of lesions. In view of difficult to manage nephritic proteinuria (daily protein depletion of 10-20 g), we decided to perform pharmacological nephrectomy and increase dehydration during dialysis. The patient made excellent progress and was discharged home 2 weeks later. He was recommended to receive doxycyclin in dose of 2 × 100 mg for 12 months. During the therapy daily diuresis decreased from 2000 ml to 350 ml.
At 12-month follow-up, the patient presented in good general condition with normal appetite and without diarrhoea. He gained 5 kg (BMI increased to 21.8) and his exercise tolerance improved so that he could get back to work. Currently, the patient is on renal replacement therapy 3 times a week with the use of arteriovenous fistula. He receives doxycyclin regularly. Control computed tomography scans showed marked reduction of abdominal lymph nodes (maximum 2 cm in diameter) ().


The patient is a 63-years-old, single, Greek female who weighs 60 kilograms (weighed 48 kilograms in 1981) and is 1.50 meters tall. She is consultant of preschool education and distinguished poet. She characterizes her current health condition as “excellent”. According to her medical case history, she had generalized ARC from 1981 (period of first diagnosis) to 1984, whereupon she was almost cured. Other health issues include primary infection by Mycobacterium Tuberculosis, without manifesting symptoms of tuberculosis, just after the appearance of ARC (1981), detection of helicobacter pylori, gastro-esophageal reflux (2003), chronic gastritis (2003), hypercholesterolemia (2003). She also underwent laparoscopic cholecystectomy (2003) after the diagnosis of acute cholocystitis. Her current medication comprises ezetimibe/simvastatin (2005) and esomeprazole magnesium (2006). She has a family history of cancer (brother, cousin, uncle) and gastro-esophageal reflux (father), but no family history of allergies. She reported neither drug nor alcohol abuse. She had been smoking 3-6 cigarettes daily from 1966 to 1996 and has been drinking 1-2 cups of coffee daily. She exercises (walking, dancing) five times a week for an hour each time.
She first developed ARC in 1981 while working in the village Katsikas near the city of Ioannina. She reports that she developed, and still has, hypersensitivity mainly to washing powder, as well as to most kinds of detergents (chlorine water, ammonia-containing solutions), every kind of dust, house dust mite and dust produced by road-traffic, gas fumes, air conditioning, pollen, scents of flowers, blossoms and plants, perfumes and synthetic aromatics. She cannot remember the exact stimuli or date of the first allergy symptoms. Describing her case, she emphasizes that her symptoms appeared all year round, not in a certain season, everywhere she was, even when she travelled somewhere or during a journey. ARC occurred after her exposure to the afore-mentioned allergens and had no connection with periods of stress or emotional discomfort. It popped up and went away, popped up, went away! “I was impressed! But, it followed me even in Russia! It was not present only in Greece. I thought that something was wrong with Greek environment!” The symptoms continued for days, weeks, or even several months and did not subside even if the allergen had retreated. She had intense watery rhinorrhea, tearing and irritation of the eyes, as well as repetitive sneezing. She also had pain, erythema and unbearable pruritus of the nose, pharynx and eyes. “Acute crises! Crises! Recurrent crises!” It was terrible! She mentioned no cough, headache, impaired smell, or nasal congestion. She said she performed allergy testing (1982) which revealed the probable allergen she was reacting to: white poplar of Belarus. “And I said that we don’t have such kind of poplar here!”
She was treated with corticosteroid pills (She cannot remember the exact name of the drug) and nasal decongestant sprays. In periods of acute exacerbation, she took the corticosteroid pills permanently. This medication pattern continued for three years. Although it was really effective in considerably reducing the allergy symptoms, the patient mentions that the action of cortisone begun only after three hours. Moreover, she noticed that she started to gain weight at the abdominal regions. This resulted in her low compliance to cortisone-including medication. “I suddenly started to gain weight. The pills contained cortisone and my doctor hadn’t informed me so.”
Though, it is highly important to evaluate the impact of her illness on her life. For her it was a painful experience, which impaired her total well-being. She had to confront recurrent crises and she often was not able to sleep at night. The symptoms were intense and she had severe physical discomfort. She was unable to work, to talk with friends, to have social life when her condition was aggravated. “I couldn’t go for a coffee and talk with friends.” Her productivity and concentration were severely restricted. “I could think of nothing else.”
The solution to her problem came really unexpectedly for her. It was a period of crisis in 1984, when she also had nausea and a feeling of stomach discomfort. Thus, she tried to drink lemon juice, hoping it would improve her abdominal pain (popular traditional therapy in Greece). Oddly enough, She noticed that her coexisting allergy symptoms improved radically! She tried it again and again and again; and in all times the result was the same. From that moment, lemon became an integral part of her life. Every time she felt that her allergy symptoms come up, she expressed juice from half or a whole lemon (half if her symptoms were relatively mild, a whole one when she was in crisis) and, then, she diluted it with a little water. Lemon brought a total change to her illness and life. Her symptoms’ intensity and incidence decreased significantly. Lemon worked in only half an hour and directly relieved her crisis. She comments that only lemon juice had this outcome. She had been drinking orange juice in rich quantities but it never alleviated the vigour of her symptoms. The consumption of lemon juice reduced her rhinorrhea, which started to give its place to a mild nasal congestion. It also reduced tearing of the eyes, sneezing, pain and pruritus. The fact is that she no longer had, nor has, crises.


A 33-year-old man presented with fever, dyspnea, and odynophagia. Five months prior to admission, the patient had been treated for dental caries at a local hospital, and at that time examination revealed seropositivity for human immunodeficiency virus. On admission, temperature was 39.0'C, pulse 92 beats per minute, respiratory rate 20 breaths per minute and blood pressure 130/80 mmHg. Physical examination revealed oral thrush, consistent with findings of extensive esophageal candidiasis in endoscopic gastroduodenscopy performed five days before admission. Laboratory data on admission revealed a WBC count of 1,760/uL, Hb 10.9 g/dL, and platelet count of 297,000/uL. Arterial blood gas analysis while breathing room air revealed PaO2 of 48.0 mmHg, PaCO2 of 32.7 mmHg, and saturation of 88.5%, and the calculated (A-a)DO2 was 53.7. CD4 count and HIV viral load were 4/uL and 130,000 IU/mL, respectively. Diffuse bilateral infiltrates of both lung fields were noted, and no cystic lesions were observed on the chest X-ray and high resolution computed tomography (HRCT) taken on admission. Bronchoscopic alveolar lavage for diagnosis of P. jirovecii was carried out, and microscopic examination of the bronchoalveolar lavage fluid obtained showed P. jirovecii; no other microorganisms were detected by culture. Treatment with trimethoprim/sulfamethoxazole, fluconazole and corticosteroids at standard dosages was started. The patient had never been on HAART therapy prior to admission. HAART therapy was added to the treatment on the 8th hospital day. During the treatment with trimethoprim/sulfamethoxazole, pancytopenia worsened. Bone marrow biopsy revealed inflamed marrow and partial necrosis. Granulocyte colony stimulating factor was used without avail. On the 22nd hospital day, the chest X-ray obtained as the patient's hypoxemia worsened revealed pneumomediastinum. HRCT showed newly formed cystic lesions in both lung fields. Pneumomediastinum was treated conservatively with high oxygen supply. CD4 cell count and HIV levels were not followed during treatment. However, as the general condition of the patient deteriorated, the patient was started on intravenous pentamidine on the 23rd hospital day. On the 25th hospital day, his oxygen requirement increased. Without intubation, as the patient and guardian refused the patient being put on a ventilator due to multiple economical and sociological reasons, the patient died on the 26th hospital day.


A 48-year-old man presented with insidious dyspnea that had developed over a period of 2 months. The patient had been seropositive for human immunodeficiency virus in 2005 in a routine physical examination for a job position as a sailor. He was on zidovudine and didanosine for 8 months but stopped taking these antiretroviral agents at another hospital for economic reasons. On admission, temperature was 38.2'C, pulse 96 beats per minute, respiratory rate 22 breaths per minute, and blood pressure 100/60 mmHg. Physical examination was normal except for decreased breathing sound in both lung fields. Laboratory data showed a WBC count of 11,010/uL, Hb 13.6 g/dL, a platelet count of 425,000/uL, and LDH of 1,095 U/L. Arterial blood gas analysis in room air demonstrated PaO2 of 54.1 mmHg, PaCO2 of 34.4 mmHg, and saturation of 89.9%, and the calculated (A-a)DO2 was 45.5. CD4 count and HIV viral load were 21/uL and 260,000 IU/mL, respectively. Chest X-ray on admission revealed diffuse ground glass opacity in both lung fields. HRCT showed interlobular septal thickening of the bronchus and bronchioles without any cyst formation (Figure ). Microscopic examination of bronchoalveolar lavage revealed P. jiroveci, and Staphylococcus aureus was detected by culture. The patient met the criteria of respiratory failure [PaO2 less than 70 mmHg or (A-a)DO2 more than 35 mmHg] and corticosteroids were co-administered with trimethoprim/sulfamethoxazole. On hospital day 4 the patient developed sudden chest pain radiating to the shoulder and neck. Chest X-ray, electrocardiography, and arterial blood gas analysis were performed. The chest X-ray revealed air lining the cardiac border, indicating development of pneumomediastinum. HRCT revealed newly developed cystic changes, bronchiectatic change, and parenchymal tear (Figure ). The pneumomediastinum was treated conservatively with administration of high oxygen supply without the need for invasive procedures. On hospital day 10, HAART was started with lopinavir/ritonavir, lamivudine, and zidovudine. On hospital day 13, follow up HRCT revealed more aggravated pneumomediastinum, bronchiectasis and parenchymal tear in the lingular division of the left upper lobe. Trimethoprim/sulfamethoxazole was changed to intravenous pentamidine. The patient experienced nausea, vomiting, and hypoglycemia on pentamidine, leading to a further change of antibiotics to primaquine and clindamycin. The patient's dyspnea improved and no particular complications were observed. The patient was discharged on the 42nd hospital day and is being followed up in the outpatient clinic.


A 33-year-old right-handed male was seen for evaluation of swelling in front of the left wrist and palm and intermittent tingling in the thumb, index finger, and middle finger that was noticed by the patient 6 months prior to seeking advice. Though the swelling had been present for a few years, the onset of tingling drew his attention.
Upon examination, there was fullness over the wrist and in the interthenar area of the palm []. Another swelling was at the base of the index finger. It was soft, non pulsatile, non compressible, and tender to touch. Tinel's sign was positive over the wrist swelling. There was no thenar wasting or sensory deficit. A radiological examination was normal. An ultrasound examination revealed a soft tissue oblong lump extending from the wrist to the palm and another separate mass at the base of the index finger. Nerve conduction studies were not performed.
Surgical exploration was performed in February 1999 under brachial block anesthesia with an upper arm tourniquet. The median nerve was found to be grossly enlarged from 4 cm proximal to the wrist crease line to the level of its division into distal branches in mid palm. Common digital nerves were not involved in the thickening. The radial-side digital nerve of the index finger was found to be merging with another fibrofatty mass at the base of the digit []. Carpal tunnel release and epineurotomy of the enlarged median nerve were Performed. A biopsy was obtained from the enlarged median nerve and the fibrofatty mass at the base of the index finger. The latter was only partially debulked for fear of damaging the digital nerve. We did not use intraoperative nerve stimulation. The wound was closed after placement of a small suction drain. The drain was removed on Day 3 and the sutures were removed on Day 14. The patient was kept on a regular follow-up schedule. Even after 5 years, the patient revealed no tingling in the thumb, index finger, and middle finger. He was able to carry out all his routine work. Upon examination, Tinel's sign was negative. Sensations were normal in the index finger and the swelling remained unchanged in size [].
The epineurotomy specimen with the biopsied strip of tissue showed minimal hypertrophy of nerve fibers. It was closely associated with a noncapsulated fibrolipomatous hamartoma, composed of a haphazard mixture of mature fibrous tissue, adipose tissue, a few blood vessels, and occasional small mature nerve twigs. The debulked mass from the base of the index finger also revealed identical features as seen in the enlarged median nerve proving both lesions to be lipofibromatous hamartoma.[] This mass was infiltrating the subcutaneous tissue resected along with the lesion. There was no neural hypertrophy or true macrodactly.


40 year old male athlete presented to the Emergency Department with pain and inability to move right shoulder. His right arm was locked in abduction of 135 degrees. The injury occurred when the patient hyperabducted his arms during a high-jump and presented with the characteristic overhead-abduction of the arm. Examination revealed loss of contour of shoulder, prominence of acromion and presence of subacromion sulcus laterally. Humeral head was palpable in the axilla. There were no neurological deficits. Brachial and radial pulses were palpable. Surprisingly, following analgesia, the patient could rest the arm at less than 90 degrees on a table (Figure ). During radiography, his arm was parallel to the chest wall (Figure ).
Detailed history revealed a similar episode of locking of the arm in the abducted position three years before while playing volleyball. However with manipulation by self, the shoulder reduced and pain subsided. General examination revealed features of generalized ligament laxity. Anteroposterior (Figure ) and modified lateral view radiographs showed inferior dislocation of right shoulder with humerus locked in adduction in the infra-glenoid region.
Under general anesthesia, on repeat examination, the humeral head was still palpable in the axilla and not anteriorly in the shoulder. Closed reduction was carried out based on the two-step maneuver described by Nho et al[].
Patient is positioned supine under sedation or anesthesia. The operator stands on the affected side, by the side of the arm (Figure ). One arm is placed on the posterolateral aspect of the mid-shaft of the humerus while the other hand is positioned over the medial epicondyle. While the second hand provides mild traction and abduction, the proximal hand gently levers the humeral head from an inferior to an anterior position relative to the glenoid. The first step is complete. Following this step, the humeral head was palpable anteriorly in the shoulder.
The proximal hand is placed on the lateral aspect of arm to adduct it against the body, while the other hand holds the forearm and externally rotates the arm (Figure ). The humeral head reduces into the glenoid. The reduction was checked with gentle passive range of motion. The arm was then internally rotated (Figure ) and shoulder immobilised in a chest-arm bandage.
Post-reduction radiography (Figure ) demonstrated concentric reduction of joint. MRI to evaluate soft-tissue injury and occult skeletal pathology revealed posterior labral tear and a bony defect on the superolateral aspect (Figure ). The shoulder was immobilized in a chest-arm bandage for 3 weeks following which he was started on shoulder, elbow and wrist range of motion exercises. At 14 weeks, he regained full range of motion and at last review at 2 years post-trauma, he was still asymptomatic.


A 62-year old man with severe back pain was admitted to tertiary care in a specialized spinal unit at the University Hospital. He complained of serious low back pain during the last 6 months without any improvement following conservative management. There was no history of trauma and the patient was neurologically intact. The serologic examination revealed an increased ESR (87 mmHg). The plain x rays (Fig ) and the MR imaging of the lumbar spine showed a pathologic fracture of the L4 vertebral body, mainly involving the superior epiphyseal plate, without extension into the spinal canal.
The preoperatively referred VAS and the Oswestry disability index (ODI) were 6 and 66% respectively. The quantity of the preoperative analgesic therapy was registered. According to the classification of Tomita et al. [], the patient had a score of 3, justifying a long term therapy. In consensus with the haematologists, a combined RFA and BKP of L4 vertebra was performed (Fig ) (see the surgical technique). The radiofrequency electrode was introduced two times in order to reach a larger necrotic area. The volume of the injected PMMA cement was 4 ml. An increase in 15% of the mid vertebral body height was observed. The histological examination confirmed the diagnosis of plasmacytoma. No complications related to procedure were observed. Postoperatively, the VAS and and Oswestry scores were 1% and 28% respectively and the patient did not need any additional analgesic therapy. In the 7-months follow-up, the patient was free of pain, the primary disease being stable with VAS and ODI being 2% and 40% respectively.


A 64-year-old man with a known liver cancer diagnosed 6 months ago, was presented to our clinic with severe pain in the lower thoracic region, deteriorating at night without any neurological deficit. He was neurologically intact. His medical history revealed a stable coronary heart disease. Histologically, the tumor was characterized as a hepatocellular carcinoma with moderate growth complicated with a treatable lung metastasis during the investigation after hospitalization. According to the classification of Tomita et al. [], the patient with 6 points in the scoring system, was an eligible candidate for a palliative surgery, aiming at short-term local control. Preoperatively his VAS score was 8 and his Oswestry low back pain disability questionnaire 84%.
The plain x-rays and the MR image show the malignant fracture at T12 level with moderate posterior bulging into spinal canal (Fig ). An additional secondary deposit is shown in the T11 vertebral body. RFA and BKP of the lesion was performed. The radiofrequency electrode was introduced two times into the body and one time in the left isthmus area of the Th12 vertebrae. The volume of the injected PMMA cement during BKP was 4 ml (Fig ). The placement of the PMMA is performed very carefully after 10 min of preparation and under continued fluoroscopic image in order to avoid the symptomatic extravasation. Increase of 8% and 11% were measured respectively for the anterior and middle vertebral wall. RFA only was performed in the T11 vertebrae and the surgical treatment was completed with the laminectomy of the T12 vertebra in order to avoid the challenging anterior approach and reconstruction in an already aggravated patient.
Immediately post-operatively, the VAS score was 4 and the need for painkillers was drastically reduced. No complications related to the procedure were observed. The VAS and the ODI at the 3-months follow-up were 2 and 52% respectively. The patient died 6 months after treatment from complications related to portal hypertension, being neurogically intact.


A 71-year-old man was admitted with invaliding, diffuse pain in the thoraco-lumbar region. The patient had reported weight loss and appetite disorders during the last 3 months. A diagnosis of diabetes mellitus type II had been established 8 years ago. The serologic examination showed hypercalcaemia (10.3 mg/dl) and increased ESR (101 mmHg). MR imaging and CT of the lumbar spine showed diffuse infiltration of the L1 vertebral body (Fig ). In addition, old osteoporotic fractures were noticed in the T12 and L4 vertebrae. The bone marrow signal intensity on T1-w images was inhomogeneous, suggesting either a chronic anaemia with red marrow reconversion or diffuse metastatic disease. Preoperatively, the VAS and the ODI were 9 and 78% respectively.
According to the classification of Tomita et al. [], the patient had a score of 4. RFA combined with BKP were planned for the T12 and L1 vertebrae and BKP alone in L2, L3 and L4 (Fig ). The radiofrequency electrode was introduced two times in order to have a larger necrosis area in both T12 and L1 vertebral bodies. In this patient, material for histopathological examination was taken before (Fig ) and after radiofrequency ablation. Radical depletion of the number of the monoclonal myelomatosus cells after the RFA with diffuse necrosis was shown (Fig ). The amount of the injected cement was 2,5 ml for T12 and L3 vertebra, 5 ml for L1, 4 ml for L2 and 2 ml for L4 vertebra.
Increases of 6% and 12% were measured respectively for anterior and middle wall of T12 vertebra and 10% and 18% were measured respectively for anterior and middle wall of L1 vertebra. 13° restoration of the kyphotic angle was observed.
An asymptomatic intravenous cement extravasation from L2 vertebra (fig ) was observed. The patient presented a low-grade fever (<38°C) for two days post-operatively without any additional symptoms and signs of infection.
The directly post-operatively VAS score was 4 whereas in the 6-month follow-up the VAS and Oswestry scores were 2% and 36% respectively, without any consumption of analgesics.


A 35-year-old male presented with dull aching left loin pain of six months duration. The pain was intermittent and nonradiating. He had no lower urinary tract symptoms, hematuria, or fever. Physical examination revealed a normal external genitalia and testes. His hemoglobin level, ESR, and urine microscopy were within normal limits. Liver function tests and chest X-ray were also normal. Contrast enhanced computed tomography revealed a 12 × 9 cm well-defined, homogenously hypodense mass arising from the lower pole of the left kidney. The mass was confined to the kidney and there was no significant perihilar lymphadenopathy [].
Intraoperatively, a 12 × 9 cm soft, yellowish mass was seen arising from the lower pole of the left kidney. The mass was excised completely with a thin rim of normal renal parenchyma.
Gross examination showed an ovoid cystic mass of 12 × 9 × 9 cm and weighing about 750 g. Cut section revealed whitish, tan and pultaceous material [].
Microscopy revealed renal parenchyma with a cystic lesion lined by stratified squamous epithelium with lamellated keratin in the lumen. Sebaceous glands were seen in the lining epithelium with surrounding adipose tissue smooth muscle. The adjacent renal parenchyma showed tubular atrophy, interstitial fibrosis, and glomerular atrophy with focal glomerulosclerosis. A few dysplastic tubules were seen in the medulla set in a fibrotic stroma [Figures and ].


A 35-year-old right-handed man who worked in a bank was admitted to hospital with complaints of neck pain and left-sided weakness. The patient had developed a sharp pain in the left side posterior aspect of his neck and occiput after a 4-hour flight, 4 weeks before presentation. At the time he felt nauseated but did not vomit, and he was treated conservatively with ultrasound and massage. The weakness began acutely after he had turned his head to one side and rapidly progressed from his left leg to his left arm. He was immediately unable to walk and subsequently began to experience tingling sensations in his right arm and leg.
There was no history of head trauma or neck manipulation, no past medical or surgical history, and no previous use of medications or previous infectious symptoms. The patient was a non-smoker, did not have diabetes and was normotensive. There was no family history of thrombophilia or venous throboembolism. Both his father and uncle had suffered from ischemic strokes in their late forties. He was born in the Philippines and had lived in Canada since early childhood.
On examination, level of consciousness, cognition and speech were normal. His blood pressure was 144/96 mmHg. The cranial nerve examination was normal. There was Medical Research Council (MRC) grade 4 out of 5 weakness affecting the left arm and left leg, with active movement possible against gravity and minimal resistance. Pinprick and temperature sensation were diminished on the right side from the second cervical vertebra (C2). Vibration and joint position were diminished on the left side below C2. The left plantar reflex was equivocal and the right was flexor. The remainder of the physical examination was normal. The results of the examination were consistent with a Brown-Séquard syndrome on the left at the level of C1-C2.
Hematologic, biochemical and immunologic investigations were normal and electrocardiogram and chest radiography were unremarkable. The lumbar puncture cerebrospinal fluid (CSF) protein was 0.22 g/l and glucose was 4.9 mmol/l (blood glucose 8.8 mmol/l). There was one white cell, two red cells, no oligoclonal banding and no xanthrochromia in 10 ml of CSF.
T2-weighted magnetic resonance (MR) imaging performed 2 days after presentation revealed a hyperintense signal associated with restrictive diffusion from the left inferior medulla and obex to the level of C2-C3, consistent with infarction (Figure ). Three-dimensional time-of-flight MR angiography showed narrowing of the left vertebral artery over the arch of C1 with a high signal parallel to the narrowed lumen, consistent with intramural hematoma and dissection (Figure ).
The patient was started on anticoagulation therapy with heparin and bridged to warfarin as secondary prevention. When the patient was discharged one month later, he was doing well, with improving, although not yet normal, strength in his left arm and leg.


A 4-month-old Egyptian baby boy was referred to Assiut University hospital by a local primary health care centre for further assessment because of his dysmorphic features and large-sized head. He was delivered at home by a midwife at full term through normal vaginal delivery. He had no prenatal or antenatal care. He was the second-born male child to non-consanguineous Egyptian parents who lived in a very small village. The couple also had a 3-year-old son who was completely healthy. The father and mother were 46 and 42 years old, respectively, at the time of the patient's birth. The mother reported that he was smaller in size at birth in comparison with his sibling. At the time of presentation, he had difficulty feeding, vomited frequently and lacked the ability to control his head. He also seldom smiled at his mother, but he had no history of convulsion or disturbed conscious level.
At the initial clinical examination, the patient weighed 4250 g (<5 centile), his head circumference was 47 cm (>97 centile) and his body length was 52 cm (<5 centile). He also had facial dysmorphism including a prominent and wide forehead, wide anterior fontanel, bushy eyebrows, synophrosis, small palpebral fissures, ocular hypertelorism, high arched palate, depressed nasal bridge, low-set ears, micrognathia (Figure ), bilateral clenched hands with overlapping fingers (Figure ), rocker-bottom feet (Figure ), and penile hypospadius (Figure ).
Cardiac examination revealed that the patient had a Grade III pansystolic murmur over his left lower sternal area with no signs of heart failure. Neurological examination revealed an increased tone in his upper and lower limbs with overactive tendon reflexes. Further tests showed that his hemogram, electrolytes, renal and liver functions, blood glucose, chest X-ray and abdominal ultrasound were all normal. Echocardiography showed that the patient had a small perimembranous ventricular septal defect (VSD). A computed tomography (CT) scan of his head showed dilatation of all the ventricular systems of his brain and suggested hydrocephalus.
A chromosome analysis (karyotyping) of the patient's peripheral blood confirmed that he had a trisomy of chromosome 18 (47, XX+18). The patient's hydrocephalus was treated with a ventriculoperitoneal shunt because of the abnormal enlargement of his head circumference. He was discharged home on nasogastric feeds at the age of 5 months. Despite the advice of the medical team, however, his patients did not bring the child for further follow up. He died at the age of 7 months due to a sudden cardiorespiratory arrest at home.


A 71-year-old Caucasian man was admitted to our hospital under the general medical team in July 2007 with a 15-month history of recurrent cellulitis over the right maxillary region of his face. There were no obvious aetiological factors apart from stable tablet-controlled type 2 diabetes mellitus. Wound swabs for microscopy, culture and sensitivity were repeatedly negative and there was no history of trauma or underlying dermatological disease. The patient had suffered from a dental abscess involving the right upper quadrant molars, but this was noted only 13 months following his initial presentation in 2006; tooth extractions performed with a view to curing his facial cellulitis had limited effect on this. Multiple courses of broad-spectrum oral and intravenous antibiotics had been ineffective in treating the cellulitis. Two computed tomography (CT) scans of the paranasal sinuses performed in February and July 2007 had ruled out sinusitis as an underlying cause. The patient had declined to have a skin biopsy.
Several days after admission, the patient developed an abscess over the right maxillary region and began complaining of a foul taste in his mouth from the discharging abscess. It was at this point that a discharging fistula between the right nasolabial fold and the right buccal sulcus was diagnosed clinically. Following reviews by clinicians in the areas of dermatology, microbiology, ENT (ear nose and throat) and maxillofacial surgery, the significance of this patient's nicorandil treatment (30 mg twice daily) initiated 4 years previously, was recognised. His drug history also included spironolactone, isosorbide mononitrate, warfarin, gliclazide, bisoprolol, paroxetine and furosemide. On direct questioning, the patient admitted to having experienced small oral ulcers involving his tongue 6 months preceding his admission, although he had not sought medical advice as they had not been particularly troubling. On this occasion, he had no oral ulcers.
On discussion with the cardiologists, the patient was put on a 4-week long tapering regimen of nicorandil resulting in complete withdrawal of nicorandil therapy. There was some clinical improvement noted at 2 weeks into this reducing regime and a month after his nicorandil therapy had ceased, his fistula had healed and the cellulitis disappeared completely for the first time in 15 months.
A retrospective review of his imaging confirmed a fistula in the right maxillary region on the CT scan performed in February 2007. The patient had not complained of any symptoms suggestive of a fistula at this point. However, retrospective questioning revealed that he had had symptoms of a 'foul taste' in his mouth during this time, which he had initially attributed to the dental abscess.
In addition, investigation of the patient's case notes revealed that he had had a persistent peri-anal fistula over a period of 1 year from 2004 to 2005. This low anal fistula was initially laid open surgically in 2004. However, this procedure was complicated by poor wound healing and abscess formation requiring two further surgical procedures over the next year. The fistula finally healed in mid-2005, corresponding to a coincidental nicorandil dose reduction from a total daily dose of 60 mg to 30 mg during the preceding month.


A 53-year-old Caucasian man presented with a two-week history of slightly scaly pruritic erythematous plaques with an orange hue that covered his face (Figure ), the extensor aspects of his arms, forearms and legs, upper trunk, buttocks and flexures. Patches of normal skin were evident within those sheets of erythema, together with prominent erythematous follicular papules at the margins of the plaques. His palms and soles were slightly hyperkeratotic with a yellowish hue. His past medical history was unremarkable. He had no arthritis, did not report symptoms or present with clinical signs that could be attributed to any autoimmune disorder. The results of his complete blood count, urine analysis and blood chemistry profile were unremarkable. Initially, antinuclear antigens (ANA) were weakly positive (1:80), later rising to high titers (1:1280) and showing a speckled pattern, whereas anti-DNA, extractable nuclear antigen (ENA), anticardiolipin antibodies and cryoglobulins were negative. C3 and C4 were mildly elevated, but CH50 was normal. The patient did not report any recent infection. Histopathology showed orthokeratosis alternating with parakeratosis, a normal granular layer, an absence of Munro microabscesses and dilatation of the dermal blood vessels with a low-grade perivascular inflammatory infiltrate (Figure , Figure ). Both the clinical and histological pictures were compatible with PRP and the patient was commenced on acitretin 50 mg/day. Within 1 month, he had improved remarkably and his skin had become almost clear. His ANA titer had decreased to 1:640 after treatment.


A 48-year-old Caucasian man presented to our clinic with a one-month history of pruritic, slowly expanding scaling lesions over his face, scalp, upper trunk and the outer aspects of his arms (Figure ). His medical history was significant for coronary disease and diabetes mellitus II. He had no arthritis, did not report any symptoms and clinical examination did not reveal signs that could be attributed to any autoimmune disorder. Physical examination revealed slightly scaling erythematous lesions over his forehead, proximal anterior scalp, the nape of his neck, face, forearms and upper trunk. The results of his complete blood count, urine analysis and blood chemistry profile were unremarkable. His ANA displayed a speckled pattern and had an initial titer of 1:640 (negative >1:80) which decreased to 1:80 positive during therapy. Ro (Sicca syndrome A; SSA) antibodies were intensively positive (145, 1 U, negative <20) and La (Sicca syndrome B; SSB) antibodies were slightly positive (33 U, negative <20). C3 was mildly increased (223 mg/dL, normal: 84, 1-167 mg/dL), whereas C4 and CH50 were normal. Anti-dsDNA, anti-RNP, pANCA, cANCA anti-Sm antibodies, as well as antibodies against histones and antibodies against cardiolipin were not identified. Direct immunofluorescence from a sun-exposed lesion did not show immunoglobulin or complement deposition. The patient did not report arthralgias, myalgias or symptoms of any other system. According to his immunological profile and his clinical presentation, the patient was initially diagnosed as suffering from subacute cutaneous lupus erythematosus (SCLE). He was started on hydroxychloroquine 200 mg per day, but the disease eruption extended to his trunk and lower extremities. Gradually, his soles and palms became intensively hyperkeratotic, salmon-colored and he developed ectropion in both eyes. The histological findings of two biopsy specimens as well as his clinical picture were compatible with PRP showing alternate areas of orthokeratosis and parakeratosis. There was no atrophy of the epidermis. His hydroxychloroquine treatment was discontinued and he was prescribed acitretin 35 mg/day and prednisolone 40 mg daily tapered progressively. The lesions improved only temporarily. Methotrexate 25 mg per week intramuscularly was added and the patient improved remarkably within 3 weeks. He is still on follow-up. His SSA antibodies remained positive (130, 2 U, negative <20) on a subsequent check while SSB antibodies were within normal limits. C3 was slightly increased after treatment (247 mg/dL, normal: 84, 1-167 mg/dL).
A diagnosis of PRP was made for both patients based on clinical and histology data.


We report the case of a 16-year-old Caucasian girl who presented to the emergency department complaining of severe nausea, epigastric pain, decreased appetite and vomiting.
Two weeks before admission, she experienced an acute onset of nausea, non-bilious vomiting, and diarrhea, which resolved within 24 hours. During the week before admission, she had an intermittent, dull, diffuse abdominal pain and decreased appetite. Over the few days before presentation, she had non-bilious emesis that progressed to bilious emesis. Her pain was non-radiating, sharp in nature and localized to the epigastric area. The pain was relieved with vomiting but it worsened after attempting to take in solids or liquids. She denied fevers, upper respiratory infection symptoms, hematemesis, hematochezia, or melena.
Further questioning revealed that during the 16 months before presentation, she had lost 22 kg (49 pounds). Upon questioning of both the patient and her mother, it was discovered that she had deliberately eliminated fat and meat from her diet and increased the amount of exercise she engaged in, including playing soccer and running. She described her body as 'sub-par' and she felt that she was challenging herself to be 'better'. She called herself a 'perfectionist' and was easily stressed out by school. However, she denied having a fixation with body image, although her mother privately reported that she had shown preoccupation with dieting, nutrition, and exercise. With her new diet and exercise regimen, she began to lose weight and she stated that she enjoyed the compliments she received regarding her physical appearance. She reported taking in approximately 900 calories per day and exercising more vigorously: she was running 3.5 miles three times a week and engaged in yoga for 1.5 hours a day on non-running days and was also playing soccer. As she continued on her diet and exercise regimen, she eventually reached a weight of 40 kg, down from her baseline of 61 kg. At that time, she was confronted by family and friends regarding her extreme thinness. She worked with her mother and her pediatrician in an attempt to increase her caloric intake and reduce her level of exercise. She acknowledged, on hospital admission, that she never ate more than 1800 calories a day, despite the agreements she made with her pediatrician and mother. Of note, she stopped having menses over a year before presentation.
Her physical examination on admission was notable for bradycardia (pulse ranging from 45 to 55), with a weight of 39 kg (z-score for age: -2.5), height of 161 cm (z-score -0.5) and body mass index (BMI) of 15 (z-score -2.9). The girl was cachectic and did not look well. Her head and neck examination was normal, including normal dentition. Her lungs were clear and she had normal respiratory effort. Her abdominal examination revealed diffuse tenderness to palpation and hypoactive bowel sounds. There were no masses or organomegaly. The rest of her examination was unremarkable.
Her evaluation in the emergency department included a barium swallow X-ray with small bowel follow-through that demonstrated an extremely dilated stomach and an inability of contrast to flow past the third portion of the duodenum (Figure ). A CT scan also revealed a dilated stomach and proximal duodenum in addition to severe narrowing of the third portion of the duodenum. Axial contrast-enhanced CT during the arterial phase clearly demonstrated compression of the duodenum between the superior mesenteric artery and the aorta (Figure ). The patient underwent immediate nasogastric tube decompression, resulting in relief of her epigastric pain and drainage of approximately 100 ml of bilious fluid. Laboratory evaluation at admission included electrolytes that were significant for a reduced chloride (95 mmol/l) and an elevated bicarbonate (36 mmol/l), consistent with emesis and a subsequent contraction alkalosis. Her amylase was 141 U/l, and lipase was 164 U/l, and her complete blood count and liver function studies were essentially normal.
After immediate decompression of her small bowel obstruction and consultation with pediatric surgery, an NJ tube was placed to provide nutrition beyond the site of obstruction. The pediatric surgical service felt that surgery would not be necessary if medical management could replete the patient's neurovascular fat stores to relieve the duodenal compression and prevent future compression. She was started on a tube feed regimen that provided 1800 kcal/day (47 kcal/kg/day), and was gradually titrated up to provide maximal caloric support, while monitoring for refeeding syndrome. Her ideal weight, based on a BMI of 20, was 54 kg, and we felt that she should regain at least 3 kg before initiation of oral feeds. The child psychiatry service diagnosed anorexia nervosa, restricting type, based on her weight restriction for 16 months, her excessive exercise, her low BMI, and her preoccupation with nutrition and exercise. They recommended transfer to an in-patient eating disorders unit, but her requirement for NJ feeds precluded this transfer. They felt that she should remain hospitalized until the NJ tube could be removed, followed by transfer to the eating disorders unit, but the patient and her family were not comfortable with this plan. Ultimately, after many multidisciplinary meetings involving nursing, discharge planners, insurance company representatives, the family, and the involved physicians, an out-patient eating disorder therapist was identified who agreed to provide regular counseling three times per week. This allowed the patient to be discharged home on tube feeds, while still receiving appropriate psychotherapy for her anorexia.
Six weeks after hospital discharge, the patient was tolerating approximately 1600 kcal/day of NJ-tube feeds and 1300 kcal/day of a diet consisting of protein shakes, yoghurt, and soft foods, without nausea, vomiting, or constipation. She transitioned to a 3000 kcal/day oral diet without difficulty and the NJ tube was discontinued shortly thereafter. Once the NJ tube was removed, she enrolled in an out-patient eating disorders day program, where she continued to receive intensive daily therapy for more than a month. She began having regular menstrual cycles again, and was able to maintain her weight at an appropriate level. One year after discharge from the hospital, her weight was 53 kg, and she remains an avid athlete and excellent student.


A 38-year-old Afro-Caribbean woman presented at 32 weeks of pregnancy with chest pain and shortness of breath. She was a non-smoker with no history of pulmonary disease. Her body mass index (BMI) was 38 and she had conceived following in vitro fertilisation (IVF) treatment. Infection screen gave negative results. On examination, she was found to be mildly tachypnoeic with decreased air entry and had a hyperresonant percussion note over the left hemithorax. Pulse oximetry showed an oxygen saturation of 95% on air. Blood gas analysis confirmed normal arterial oxygen and carbon dioxide tension. Chest X-ray revealed a large left pneumothorax with a collapsed lung (Figure ).
On examination and ultrasound scan, uterine fibroids were diagnosed with the largest one measuring 22 cm. She had problems with fibroid degeneration and dental abscess during this particular pregnancy.
Pneumothorax was treated using chest tube drain, and it resolved completely in a few days (Figure ).
She was readmitted with another pneumothorax two weeks later and on the 34th week of gestation. A chest drain was reinserted and removed three days later following resolution of the pneumothorax.
Unfortunately, the pneumothorax recurred after another three weeks and a chest drain was again inserted (Figure ).
She had also started developing pre-eclampsia when she was nearly 37 weeks in her pregnancy. Labour was induced at this stage. She had an epidural during labour. She had normal vaginal delivery with the baby born in good condition and weighing around 2760 gm.
The chest drain was removed after delivery, and this was followed by video-assisted thoracoscopic surgery (VATS) and apical pleurectomy.
The postoperative period was uneventful and she made a smooth recovery.


A 51-years-old Pakistani male, without any known medical co-morbidity, presented to the emergency department at our institution with a 1 day history of sudden-onset and severe abdominal pain along with abdominal distension. The pain had started after a long drive of 12 - 14 hours. It was initially localized to the right upper quadrant and right lumbar region but had evolved to a more generalized distribution over time. The pain was aggravated on movement and relieved by rest. There were no other associated symptoms. His past surgical history was significant for a repaired left sided inguinal hernia 10 years back.
The patient was in obvious anxiety and distress when first encountered in the emergency room. His vital signs were stable except for an increased pulse of 105 beats per minute. Examination of his respiratory system revealed vesicular breathing with decreased intensity of breath sounds in the right lung base as well as dullness on percussion on the right side of the chest. His abdomen was distended with generalized tenderness on palpation and minimal movement with respiration. No organomegaly was appreciated on the physical examination. His bowel sounds were sluggish.
The laboratory tests done at the time of admission are shown in table . The patient had mild anemia, mildly reduced hematocrit, leukocytosis with neutrophilia and hyponatremia. His serum amylase, lipase and random blood sugar levels were all within normal limits. His abdominal x-ray showed sub-optimal inspiration with minimal right sided pleural effusion. However, there were no signs of intestinal obstruction or pneumoperitoneum noted. Subsequently, computed tomography (CT) scan of the abdomen was done. Gallbladder margins were not very clearly identifiable; there was significant pericholecystic fat stranding with pericholecystic fluid. A circular high density focus in the proximity of gallbladder was identified which was thought to be representing a gallstone. Mild ascites was also present. These features were collectively suggestive f gallbladder perforation. (Figures and )
The patient's emergent management included nothing per oral status, regular vitals and input/output charting, insertion of nasogastric tube, administration of intravenous fluids, narcotic analgesics, proton pump inhibitors, metochlopramide, ceftriaxone, metronidazole, and ampicillin.
The patient was then taken to the operating room and a diagnostic laparoscopy was performed. It revealed free yellowish green fluid, most likely bilious, in the peritoneum. As the triangle of Calot could not be identified on laparoscopy, the procedure was converted to an open laparotomy. Intra-operative findings included presence of frank bile in the abdomen and a thick walled gall bladder. Dense adhesions of the gall bladder with surrounding structures were observed. A small perforation was visible near the neck of gall bladder in association with a large gall stone. The anatomy of the Calot's triangle was still obscure. A near-total or partial cholecystectomy including the perforated area was performed and a single large gall stone measuring around 2 × 1 cm was retrieved. The peritoneal cavity was washed with copious amounts of normal saline and a drain was placed. The rectus sheath was closed with loop polydioxanon (PDS) but the wound was kept open for healing by delayed primary closure.
Histopathology of the specimen showed full thickness gallbladder wall lined by mucosa with focal ulceration. Rokitansky aschoff sinuses were also seen. A pathological diagnosis of acute on chronic cholecystitis was made.
The patient's hospital course was uneventful. His symptoms significantly improved and he was discharged from the hospital on the third post-operative day. He returned to the clinic after one week when his drain was removed and his wound closed.


A 15-year-old English Caucasian male was brought to our emergency department having suffered a witnessed cardiac arrest, following the use of alcohol and cannabis with friends. Paramedics attended the scene within three minutes of call being passed: cardiopulmonary resuscitation (CPR) was in progress by the patient's friends, and the first recorded rhythm was asystole. After two minutes of CPR, the rhythm changed into ventricular fibrillation (VF) which was successfully cardioverted into a sinus rhythm with a single DC shock (200 J).
On arrival to hospital, the patient was maintaining his airway with respiratory arrhythmia. His vital signs showed a blood pressure (BP) of 115/86, a heart rate (HR) of 86 bpm and a recorded GCS of 4 out of 15. In view of the respiratory arrhythmia and impaired GCS, he was intubated and ventilated.
Investigations conducted in the emergency department showed the initial 12-lead electrocardiogram (ECG) to be in a normal sinus rhythm without any acute ischaemia. No changes were identified on subsequent 12-lead ECGs. Urine drug screen (Princeton BioMeditech Corp., AccuSign® DOA 4) was positive for THC, but negative for opiates, amphetamines and cocaine. Blood tests including haematology, biochemistry and gases were all within normal.
Radiological imaging revealed normal chest X-ray and computed tomography (CT) scan of the head. Of note, the patient had an episode of significant bradycardia whilst being scanned that necessitated a dose of intravenous Atropine.
Further information obtained from social workers disclosed the patient to suffer from attention deficit disorder (ADHD) along with a history of previous cocaine and ecstasy abuse. Although Ritalin was prescribed for his ADHD, he had failed to comply with the treatment in the last 18 months.
Our patient was admitted to a paediatric intensive care unit (PICU) at a neighbouring hospital. He was successfully extubated within 24 hours, and discharged from hospital 5 days later with no neurological or cardiovascular sequelae. Although arrangements were made for an outpatient follow up, he failed to attend his appointments and further cardiological assessments (such as echocardiography) never materialised.


A 55-year-old female presented with history of progressively increasing dysphagia for solid foods for the past six months. She was a known case of oral lichen planus and was on treatment with steroids for the past five years. The patient did not have any history suggestive of gastroesophageal reflux or any history of intake of drugs known to cause esophagitis.
Barium swallow was done which showed a long segment benign stricture of the upper thoracic esophagus [ and ]. Subsequently endoscopy showed narrowing of upper thoracic esophagus and the scope could not be negotiated distally. The mucosa proximal to the stricture showed erosions. Biopsy taken from this region showed inflammatory cell infiltrates with lymphocytes. Based on the history, barium and endoscopic appearance and the biopsy finding, a diagnosis of esophageal lichen planus was made. Patient underwent endoscopic dilatation in three sittings and her symptoms improved.


A 60-year-old woman presented to our medical center for evaluation of acute onset headache and confusion. Her past medical history was remarkable for alcoholic cirrhosis and hepatitis C. Physical examination revealed the presence of mild ascites and hypoxemia (91%) on room air with no response to supplemental oxygen. Noncontract head CT was without focal abnormality, but cerebrospinal spinal fluid analysis showed xanthrochromia suggestive of subarachnoid hemorrhage. Catheter angiography of the cerebral vessels confirmed the presence of a right middle cerebral artery (MCA) aneurysm, and the patient underwent endovascular coiling without complication. Postprocedure day number two, the patient decompensated and developed respiratory and congestive heart failure. A right internal jugular catheter was placed for venous access and hemodynamic monitoring. Daily surveillance transcranial Doppler (TCD) and noncontrast head CT showed no abnormality until postprocedure day number four when embolic signatures were detected in the basilar and bilateral MCAs. Given the multiple vascular territories involved in the ultrasound findings, a search for the source of emboli was initiated. The patient was unable to undergo transesophageal echocardiogram due to the presence of varices, but transthoracic echocardiogram with agitated saline contrast was performed while mechanically ventilated and repeated once she was extubated. No patent foramen ovale was identified, but a large amount of echogenic contrast was detected in the left atrium after 3-4 heartbeats. The delayed appearance of saline contrast in the left atrium and its origination from the right pulmonary vein were anatomically consistent with shunting through the pulmonary circuit, and similarly confirmed by TCD. The patient was started on daily antiplatelet therapy with 325 mg aspirin and the embolic signatures on TCD ceased within three days. She soon recovered from the events surrounding her hospitalization, however suffered a fatal intracranial hemorrhage five months later.


A 23-year-old Caucasian male patient consulted the Department for Cranio- and Maxillofacial Surgery for analysing an intraosseus, rounded tumour in the left mandibular corpus, which was initially diagnosed by an MRI scan 12 months ago in a different institute (Fig. ). This MRI was part of a routinely follow-up, since 10 years before two intracranial, solid and non-proliferating soft-tissue-tumours were diagnosed in the right cerebellar hemisphere (close to the foramen magnum) and underneath the left temporal lobe. Additionally, two years later an extensive but low-grade myofibroblastic sarcoma in the right ramus of the mandible was resected. A current panoramic radiography (Fig. ) showed a well circumscribed, rounded osteolysis with a diameter of 13 mm in immediate proximity to the left mental foramen. Besides, the known and in size constant translucency within the right ramus (after sarcoma-resection 8 years before) appeared inconspicuously. There were no other pathological findings.
As therapy a paramarginal approach showed the intact vestibular cortical surface with an inconspicuous mental foramen and a normal structured mental nerve. The osteotomy exposed a rounded cavity, in which a 1.3 × 0.9 × 0.6 cm sized, greying, tubercular, firm-elastic conjunctive-tissue-tumour was located. This tumour showed a very slight adherence to the surrounding bone and was resected easily. After that the bone cavity was carefully reamed under preservation of the mental nerve. Because of the small defect-size any bone-grafting material could be dispensed. The histopathological examination revealed a mesenchymal tumor, composed of spindle-shaped cells with myofibroblastic differentiation, abundant collagen formation and low proliferation activity (Fig. and ). In immunohistochemical stainings the tumour-cells showed a positive reaction for smooth muscle actin and a negative reaction for S100 (data not shown). With the proliferation marker Mib1 less than 5% of the tumour-cells proved to be positive. Based on these characteristics the diagnosis of a desmoplastic fibroma was made, and this diagnosis was confirmed by a reference institute. The post-operative recovery was normal based on clinical examination The radiographical (panoramic X-ray) follow-up showed an obvious ossification of the former resection cavity (Fig. ) and the patient described no hypaesthesia of the mental nerve at any time.
In conclusion the Desmoplastic fibroma (DF) is a rare, benign but locally aggressive, intraosseous lesion with a high tendency of local recurrence. With respect of the patient's post-operative well-being and if periodic follow-ups are guaranteed, the tumor should be carefully resected with only narrow safety margins.


A 20-month-old male child was admitted with complaints of dry cough, dysphagia, and low-grade fever of one-month duration. There was no abnormality detected on clinical examination. On investigating the child, his Hb was 10.8g%, WBC – 9,700, S. LDH – 356, LFT and RFT were normal. An x-ray chest revealed superior mediastinal widening []. HRCT chest showed a lesion in the posterior mediastinal region with mass effect on the esophagus and trachea and a normally placed thymus which was enlarged but normal for age. The most common differential diagnosis of this mass – neuroblastoma was suspected and child investigated for the same. All investigations including MIBG, Urinary VMA, and serum alpha-fetoproteins were normal. In view of the obstructive symptoms excision of the mass was planned. At right posterolateral thoracotomy through fourth intercostal space, a nodular mass was found behind the trachea extending up to the carina not communicating with any other structure. A normal thymus was found in the anterior mediastinum. The posterior mediastinal mass was completely excised after careful dissection of the trachea, esophagus and the nerves and sent for histopathology, which revealed normal thymic tissue.
Post-operatively, the child developed right phrenic nerve neuropraxia causing asymptomatic right eventration of diaphragm. The child was followed up for 4 years. An x-ray chest done 1 year later showed complete resolution of the eventration and the latest x-ray 6 months ago was also normal.


A 44 year-old Caucasian man with chronic hepatitis C infection and known, long-standing primary hypothyroidism presented with recent onset Graves' ophthalmopathy (GO). There was no other medical problem and the patient had otherwise been well. His hypothyroidism was diagnosed 10 years prior, approximately at the same time as his hepatitis C. At that time, the thyrotropin (TSH) was found to be 34 IU/L, free tetra-iodothyronine (fT4) 10.2 and free tri-iodothyronine (fT3) 3.2 pmol/L. He was started on thyroxine therapy with subsequent satisfactory control. No information on autoantibodies or imaging was available from this presentation.
Clinical examination showed a tattooed man in euthyroidism. His ophthalmopathy was graded as moderate-to-severe including >3 mm lid retraction and marked congestion with a clinical activity score (CAS) of 5/7 []. Visual acuities were 6/6 bilaterally. No goitre, dermatopathy or acanthosis nigricans was detected. His liver span was normal at 11 cm and there was no evidence of chronic liver disease, ascites or portal hypertension. His thyroid ultrasound scan showed 2 small nodules but was otherwise normal in volume. His thyroid pertechnetate uptake scan was reduced at 1% (reference range (RR), 3-8%) whilst on 150 μg of thyroxine daily, at which time his TSH was 1.98 (RR, 0.4-4.0 mU/L) and fT4 21.5 (RR, 10.2-24.5 pmol/L). His antithyroperoxidase and antithyroglobulin antibodies were undetectable. The thyrotropin receptor antibody (TRAb) was 4.0 IU/L (reference interval, < 1.0 IU/L). Other routine laboratory tests were normal including aspartate and alanine aminotransferase activity. His baseline viral load was 6.08 log IU/mL. His ocular magnetic resonance imaging (MRI) supported the diagnosis of GO (Figure ).
Due to the diametrically opposite clinical findings of hypothyroidism and GO, further bioassays were performed to assess antibodies affecting the function of the TSH receptors. The thyrotropin stimulating antibody (TSAb) was 192 (RR, <180%) and thyrotropin blocking antibody (TBAb) 124 (RR, <40%), suggesting that the mechanism for his hypothyroidism was immune mediated with TSH blocking activity.
Due to the presence of hypothyroidism and the potential additional effect of interferon on thyroid tissue, hepatitis C treatment was carefully started. Because of his hepatitis C genotype 2, liver biopsy was deemed unnecessary and thus was not performed []. Treatment then included combination interferon-α and ribavirin for 24 weeks. The ophthalmopathy did not worsen and was managed conservatively with liquid film eye drops and protective glasses. The CAS remained unchanged. Both his eye and thyroid status was monitored and closely reviewed every month. On the 8th week, his TSH declined, necessitating a reduction in thyroxine dosage. At 16 week, he was found to be biochemically thyrotoxic with suppressed TSH, fT4 of 28.9 and fT3 of 6.9 pmol/L at which time his thyroxine was ceased. The TSH stimulating activity increased whilst blocking activity declined. His TSAb rose further whilst blocking activity declined. The evolution of the antibody profile is summarised in Figure . The thyroid uptake scan evolved to show a diffuse and increased in uptake at 12%. The potential and aggravating effects of elevated TSAb titres on the ophthalmopathy were duly considered but observation was continued (see below).
As the patient was asymptomatic, his thyroid condition was also observed closely. His serial fT4 and fT3 levels remained high but unaltered throughout the course of therapy (Figure ). Four weeks after the completion of therapy, his TSH was 0.05 mIU/L, fT4 21.5 and fT3 4.9 pmol/L. At 12 weeks, his level had become progressively hypothyroid with TSH of 5.9 mIU/L and fT4 17.9 pmol/L. At the subsequent 6, 12, 24 and 36 months follow-ups, his TSH levels ranged between 5.3 and 6.4 mIU/L. His viral load was undetectable at the 6-month follow-up consistent with sustained virologic response.


A 20-year-old man was admitted to a psychiatric ward due to depressive mood of bipolar I disorder. The WBC count and absolute neutrophil count (ANC) at the time of admission were 4,400 cells/mm3 and 2240 cells/mm3, respectively.
On day 2, treatment with lamotrigine (12.5 mg/day) and amisulpiride was initiated and the lamotrigine was increased to 75 mg/day after 4 weeks with 200 mg of amisulpiride. Fluoxetine was prescribed at week 5, along with increasing the dose of lamotrigine to 100 mg/day by week 6.
A CBC at the 45th day after starting the lamotrigine revealed a WBC count of 2,390 cells/mm3 and an ANC count of 574 cells/mm3. The lamotrigine was discontinued immediately, while the other concurrent drugs were maintained. At the next day, a CBC revealed an ANC count of 380 cells/mm3 with agranulocytosis. Although there were no signs of infection, we injected 30 µg of G-CSF and filgrastim, after consulting a hematologist. An ANC count on the 6th day after lamotrigine discontinuation was 3,503 cells/mm3 with a normal WBC count ().


A 19-year-old woman was treated for bipolar II disorder with quetiapine, paroxetine, trazodone, and valproic acid for about 6 months before admission. During this period, she presented with mild neutropenia (ANC count: 1000-1500 cells/mm3), and the cause of this was assumed to be the valproic acid. After the valproic acid was discontinued about 3 months before admission, her ANC count was normalized.
Due to the aggravation of her suicidal ideation, she was admitted and then started on 25 mg of lamotrigine. A CBC done at the time of admission showed a WBC count of 4,900 cells/mm3 and an ANC count of 2,328 cells/mm3. Neutropenia manifested on day 14 (an ANC count of 1,282 cells/mm3), but upon consultation with a hematologist, the lamotrigine prescription was continued upon consideration of her previous history of persistent neutropenia. On day 24, her ANC count was reduced to 720 cells/mm3, so on day 26, the dosage of lamotrigine was reduced to 12.5 mg/day. But on day 27 there was an outbreak of agranulocytosis (ANC count: 491 cells/mm3), and the lamotrigine was discontinued immediately (concurrent medications: 5 mg of olanzapine, 200 mg of quetiapine and 50 mg of trazodone) (). On the 7th day after lamotrigine discontinuation, her ANC count (2,330 cells/mm3) was normalized ().
Due to her severe suicidal ideation, clozapine was initiated about 33 days later and the lamotrigine was reintroduced approximately 100 days after its discontinuation. Now, about 27 months later, she is on 300 mg of lamotrigine and 262.5 mg of clozapine without any hematologic abnormalities.


A 27-year-old man had been taking risperidone for 6 years for the treatment of bipolar I disorder. He was admitted due to a depressive mood and auditory hallucinations. A CBC done on admission day showed a WBC count of 12,670 cells/mm3 and an ANC count of 9,541 cells/mm3. The patient was started on lamotrigine (25 mg/day) and this was increased to 100 mg/day 18 days later. On the 20th day, 12.5 mg of clozapine was added and a CBC revealed a WBC count of 6,510 cells/mm3 and an ANC count of 3,431 cells/mm3.
On the 29th day after lamotrigine initiation (the 9th day after clozapine initiation), a CBC revealed an ANC count of 348 cells/mm3 with agranulocytosis (concurrent medication: 4 mg of risperidone and 175 mg of clozapine). The lamotrigine was discontinued immediately. On the 3rd day after discontinuation, the patient's ANC count increased to 2,367 cells/mm3 (). Afterwards, the risperidone was discontinued, and the dosage of clozapine was increased to 225 mg, and there have not been any hematologic abnormalities since then.


A 2-month-old female weighing 3.5 kg was referred to our centre with clinical signs of congestive heart failure. Shortly after birth, diagnosis of ventricular septal defect (VSD) was made. Due to failure to thrive, the baby underwent echocardiographic evaluation that revealed a mitral valve dysplasia compatible with hammock mitral valve with remarkable alteration of the subvalvular apparatus leading to severe stenosis. The mean gradient across the mitral valve was 20 mmHg. A 5 mm perimembranous VSD was also present. The clinical conditions were critical despite full medication and surgery was undertaken. A mild hypothermic cardiopulmonary bypass was established and direct inspection after trans-septal approach confirmed a very dysplastic valve absolutely unsuitable for repair. Perimembranous VSD was closed with bovine pericardial patch (Periguard; Bio-Vascular Inc., St. Paul, Minn, USA). The mitral valve was removed leaving a 12 mm diameter anulus incompatible with a intra-annular mechanical valve implant. The pulmonary valve was inspected and harvested with 3 mm infundibular muscular rim; the pulmonary trunk was sectioned just above the commissures. The pulmonary valve sized 10 mm and was mounted inside a 10 mm long woven Dacron tube graft of 12 mm of diameter (Vascutek, Renfrewshire, Scotland). The proximal and distal ends of the pulmonary autograft were then secured to the Dacron graft with three Prolene 7/0 running sutures respectively (Ethicon, Somerville, NJ, USA). The prosthesis was therefore doubly longitudinally incised to allow autograft grow and then implanted in the mitral anulus with 5/0 Prolene (Ethicon, Somerville, NJ, USA) interrupted stitches secured at the distal edge. A top-hat valve with pericardium, as recommended by Kabbani et al. [], Ross and Kabbani [], was not feasible for the small dimension of the left atrium. At the end of the procedure, valvular continence was optimal at saline injection (). Right ventricular outflow tract was reconstructed with a 12 mm Contegra conduit (Medtronic Inc, Minneapolis, Minn, USA). At CPB suspension, persistent pulmonary hypertension was evident and inhaled NO therapy was started and switched to oral sildenafil 5 days later. The baby was discharged without complications and after 4 months, the echocardiogram showed trivial autograft gradient with no incompetence (). 3D echocardiographic evaluation confirmed the good motion of the pulmonary autograft leaflets.


A 24-year-old female presented with a swelling in the right breast of 4 days' duration. There was no history of fever. USG showed a cystic lesion at the 9 o'clock position (i.e., in the medial quadrant). The cyst wall was very thin and debris was seen in the dependant part of the cyst []. A tube-like structure was seen eccentrically within the cyst []. On questioning, the patient revealed that she had a history of tuberculous meningitis for which she had been treated with antituberculous medication and a ventriculoperitoneal (VP) shunt. She denied any recent breast surgery, trauma, or mammography. In view of the history and the USG findings, a diagnosis of CSF pseudocyst was considered. This was confirmed at surgery, during which infected fluid was drained and the shunt tube was removed.


A 21 year-old female married at the age of 18 years attended the Institute of Reproductive Medicine out patient clinic with secondary subfertility of 2 years, irregular cycles and polycystic ovaries.
The patient had already undergone five cycles of ovulation induction (clomiphene citrate and gonadotropin) with intra-uterine insemination (IUI) and laparoscopy showing bilateral sacculation of tubes with slow spill at both ends.
Obstetric history included missed abortion at 8 weeks of gestation, 2 years back.
There was no past history of chronic pulmonary obstructive disease, asthma or tuberculosis.
Also, there was no family history of any chronic illness, including thrombo-embolism.
Clinical examination showed a body mass index of 24 kg/m2 and no evidence of hyperandrogenism.
Pelvic ultrasound scan revealed polycystic ovaries and a normal-sized anteverted uterus. A baseline hormonal profile performed on day 2 of the menstrual cycle showed a follicle- stimulating hormone (FSH) concentration of 4 miu/ml, luteinizing hormone concentration of 6 miu/ ml and an estradiol concentration of 32 pg/ ml. The total antral follicle count was 24, with a right ovary volume of 11 cc and a left ovary volume of 12 cc. The husband's semen analysis showed normozoospermia.
The patient was planned for ovulation induction with IUI, explaining the risk of hyperstimulation and thereafter converted to IVF. She underwent controlled ovarian stimulation according to the flexible gonadotropin-releasing hormone antagonist protocol. She was started on a low- dose injection of hp FSH 75U (Bravelle; Ferring Pharmaceuticals, [India]). The dosage was increased to 150U after 6 days of gonadotropin as there was no response. A scan done after 2 days showed recruitment of more than six follicles and, after recounselling, was converted to IVF cycle. When three follicles reached a mean diameter of ≥18 mm (folliculogram: ≥14 mm, eight follicles; 10-14 mm, three follicles; < 10 mm, four follicles), the patient received 10,000 units of urinary human chorionic gonadotropin (hCG) (Choragon; Ferring Pharmaceuticals). On that day, her estradiol was 1272 pg/ml. Ten oocytes were retrieved, of which seven fertilized. On day 3, three grade A embryos were transferred and the remaining four were cryopreserved.
The patient presented with breathlessness and orthopnea 11 days after embryo transfer (day 16 post hCG). There was no history of fever, cough or chest pain.
On examination, her pulse rate was 90/min, blood pressure 120/70 mmHg, temperature 37°C and respiratory rate 24/min. On chest auscultation, decreased breath sounds at the basal area of both the lungs with occasional crepitations were heard. The abdomen was soft, bowel sounds were present and there was no clinical evidence of ascites.
Ultrasonography (both transvaginal and transabdominal) of the abdomen and chest showed bilateral enlarged ovaries (90 × 85 mm and 85 × 54 mm) with no fluid collection in the pelvis. However, there was evidence of bilateral pleural effusion. The oxygen saturation on air measured with a pulse oximeter was 96%. Laboratory investigation revealed a hematocrit value of 34% and white blood cell count of 11,000 cells/cub.mm. βhCG was 236 miu/ml (11 days post-embryo transfer). Her renal and hepatic parameters were normal.
Echocardiography (Echo) showed good LV function with mild pericardial effusion.
Provisional diagnosis of bilateral hydrothorax secondary to late onset OHSS.
The other differentials considered were tuberculosis and pulmonary embolism.
Tuberculosis was considered because of its high prevalence in India. It was ruled out as the patient presented with short history, with no constitutional symptoms, no history of exposure or family history and routine chest X-ray performed at the time of laparoscopy was normal.
The patient's condition was stable and oxygen saturations were maintained.
She was managed conservatively with a multidisciplinary approach and intensive care monitoring. She was placed in a propped-up position along with chest physiotherapy, intermittent O2 inhalation and nebulization.
Echo and ultrasound scan later confirmed resolution of pericardial and pleural effusion.
Fortunately, the patient did not require thoracocentesis as her symptoms subsided. She was discharged after 1 week and repeat investigation revealed doubling of serum βhCG.
Transvaginal ultrasound performed 1 week later showed twin intrauterine gestation, which is ongoing.


A 62-year-old lady was found wandering in the premises of a famous temple town in Kerala. When the local police questioned her, she said that she had left her home a few days ago and would now like to return. She provided them with the telephone number and address of her residence based on which the police were able to reunite her with her family.
On her return, the family discovered that she quickly got back to her old household routine, but was unable to remember people (neighbors, local shopkeeper) and events that had taken place in the preceding weeks. She was also confused about where she had gone and what she had done when she left home, but was able to furnish proof that she had traveled by train to a temple in a neighboring state, where she had spent her childhood. As they could not understand her patches of memory loss, the family brought her for a neurological evaluation.
An interview revealed that she was treated in the outpatient unit of the hospital for a fall six weeks ago. She had fallen from the pillion seat of a scooter and had been brought to the Casualty Section for first aid. There was no loss of consciousness, headache, blurring of vision, or vomiting. She was evaluated as an in-patient for possible post-traumatic sequelae. Medical examination revealed that she was hypertensive, but not on regular treatment. A neurological evaluation at that stage revealed no anomalies in her cognition or behavior. The CT scan and profile on blood investigations were within normal limits.
On this follow up, the Mini Mental State Examination score was 27. With no neurological problems elicited on examination and investigation, a working diagnosis of pseudo-dementia was made and a course of anti-depressants was prescribed.
On follow up, there was improvement in her mood, but the amnesia persisted. She was therefore referred for evaluation, to the clinical psychologist.
In this patient, there were no neurological or behavioral symptoms in the immediate post-traumatic period, except for mild features of a depressive disorder. The question here would be whether absence of “positive findings” could truly rule out organic causes for such impulsivity in behavior. A referral to the mental health practitioner is sometimes a resisted step in the treatment process, especially in a country such as India. It is only when the investigations rule out organicity, that “psychogenicity” of a symptom is considered.
In appearance, she was an obese lady who appeared anxious and tearful. She was initially unwilling to answer questions and repeatedly said that she could not remember what had happened. Speech was slow, but relevant and coherent. Mood was depressed; there was guilt and ideas of hopelessness. There were no hallucinations or delusions. Apart from deficits in semantic memory, there were no anomalies in primary mental functions.
On account of her apparent distress while answering questions, sessions of hypnosis were attempted. However, we encountered resistance and therefore, a supportive client-centered approach was adopted, with which she appeared to be more comfortable.
Formal psychometric assessment was deferred, in favor of serial Mental State Examinations.
Over the next three sessions, she was able to recall incidents of the preceding weeks. The most distressing episode according to her was the argument she had had with her husband. She felt that despite decades of managing the household and coping with several psychosocial stressors, the husband was overly critical of her. She described the intense grief she experienced that had prompted her to walk away from home. She visited several local temples before boarding a train to a famous temple town. After a day's stay there, she traveled by train to a temple in a neighboring state. It was the first time she was traveling alone by train, and she reported that she traveled ticketless on certain parts of the travel. She reported that she did not plan her movements, but seemed to instinctively move from one place to the other. It was only upon her return to her home state, after a few days that her memory “returned” and she went up to a local policeman and asked for help. She reported feeling very guilty over her “flight,” but insisted that there was no deliberate attempt to cause distress to her family. She did not remember people whom she was in contact with, during the travel, but could produce some of the tickets she had used. She had a purse with some money, but had pawned jewellery to purchase clothes and a few other necessities for herself. On her return, she was also very perplexed about the identity of some of the people around her and did not understand why she could not identify them.
There had been no incidents of similar behavior in the past; there were no reports of seizures, somnambulism, or other parasomnias. There were no differences in behavior and cognitive functions following the injury. The family described her as a quiet, responsible individual who had efficiently managed the household. Prior to her flight, she had participated actively in a family function; on her return, despite several cues, she could not recall the event or her family members who had reunited after a long while.
We considered the diagnosis of fugue because of the organized flight from home with significant disruption of her social and occupational routine, as also the absence of pre-morbid neurological or psychiatric problems and the self-remitting course of the altered behavior. The amnesia noted on her return was episodic and circumscribed (restricted to a few select people). The odd points in the case were the age and the absence of severe psychological trauma that could have precipitated the flight.
As we report the case, the client has returned to her pre-morbid level of functioning and comes regularly for follow up. She continues to be on a mild course of anti-depressants and supportive therapy. We plan to monitor her cognitive and psychiatric status over regular follow-up sessions and taper the sessions gradually if she maintains this improvement.