Mild Normocytic Anemia Research Articles

Prevalence and Predictors of Maternal Anemia during Pregnancy in Gondar, Northwest Ethiopia: An Institutional Based Cross-Sectional Study.

Background. Anaemia is a global public health problem which has an eminence impact on pregnant mother. The aim of this study was to assess the prevalence and predictors of maternal anemia. Method. A cross-sectional study was conducted from March 1 to April 30, 2012, on 302 pregnant women who attended antenatal care at Gondar University Hospital. Interview-based questionnaire, clinical history, and laboratory tests were used to obtain data. Bivariate and multivariate logistic regression was used to identify predictors. Result. The prevalence of anemia was 16.6%. Majority were mild type (64%) and morphologically normocytic normochromic (76%) anemia. Anemia was high at third trimester (18.9%). Low family income (AOR [95% CI] = 3.1 [1.19, 8.33]), large family size (AOR [95% CI] = 4.14 [4.13, 10.52]), hookworm infection (AOR [95% CI] = 2.72 [1.04, 7.25]), and HIV infection (AOR [95% CI] = 5.75 [2.40, 13.69]) were independent predictors of anemia. Conclusion. The prevalence of anemia was high; mild type and normocytic normochromic anemia was dominant. Low income, large family size, hookworm infection, and HIV infection were associated with anemia. Hence, efforts should be made for early diagnosis and management of HIV and hookworm infection with special emphasis on those having low income and large family size.

Massive diverticulosis of the small intestine

A 72-year old man presented with a 6-month history of weight loss (approximately 27kg), diarrhoea (up to 12 loose stools/day) and bloating. He was severely malnourished and had moderate pretibial pitting oedema. On examination of the abdomen borborygmi and succussion splash were noted. Blood work revealed mild normocytic normochromic anaemia, hypoalbuminemia and a low cholesterol level. The stool test showed undigested muscle fibres and starch but no neutral fat or fatty acid crystals.

Endoscopic Diagnosis of Hookworm Infection in a Previously Deployed U.S. Military Member

Purpose: Hookworms are soil-transmitted intestinal helminthes and are a primary cause of iron deficiency anemia worldwide, with an estimated global prevalence of nearly 750 million infected persons. We report a case of a U.S. military service member with an endoscopic diagnosis of Ancylostoma duodenale during an evaluation for iron deficiency anemia. Case: A 24-year-old active duty male deployed in 2011 in support of Operation Enduring Freedom in Afghanistan sustained an improvised explosive device (IED) blast injury complicated by an open left foot fracture and pseudomonas aeruginosa osteomyelitis following internal fixation. He initially had mild anemia attributed to polytrauma and osteomyelitis, but, additionally, was noted to have a peripheral eosinophilia of 3706/mcL. A subsequent serologic parasite work-up was negative, as were stool examinations for ova and parasites. He had persistent mild normocytic anemia through 2012 after an elective left below-the-knee amputation for ongoing complications. He re-presented in 2013, complaining of fatigue with vigorous physical therapy. At that time, he had severe iron-deficiency anemia, with hemoglobin 6 g/dL, MCV 66 fL, iron 14 mcg/dL and ferritin 1.8 ng/mL, and ongoing eosinophilia of 2414/mcL. Colonoscopy demonstrated numerous 1.5-cm long worms. Based on exposure in Afghanistan, severity of progressive anemia, gross examination, and four hook-like teeth at the caudal end of the adult worm, Ancylostoma duodenale infection was diagnosed. The patient improved, following treatment with albendazole and iron replacement. While well-described hookworm outbreaks occurred in U.S. forces during the Second World War and, more recently, in Grenada, hookworm infections are rare in contemporary military operations. There are no prior documented cases of Ancylostoma infection in military service members returning from U.S. operational support in the Middle East or central Asia. Comprehensive public health and hygienic practices are necessary to prevent this and other enteric diseases in the deployed setting.Figure: Hookworms visualized during colonoscopy. A worm was removed via biopsy forceps to facilitate identification.

Castlemanʼs Disease: One Step Beyond Kaposiʼs Sarcoma

Purpose: A 27-year-old male with a history of HIV (CD4 count 124, viral load 603,600) presented with a two-month history of fatigue, subjective fevers, decreased appetite, and a 70-lb weight loss over the past year. His physical exam was significant for diffuse bilateral cervical lymphadenopathy, bilateral supraclavicular, and bilateral inguinal lymphadenopathy. Labs revealed a mild normocytic anemia (Hgb 12 g/dL), WBC 6.5 (monocytes 26%), normal liver enzymes, and a negative hepatitis panel. A PET CT showed extensive, widespread active lymphadenopathy throughout all lymph node groups above and below the diaphragm. He underwent an excisional biopsy of the left inguinal lymph node. A colonoscopy was performed to evaluate reported constipation and rectal bleeding. The colonoscopy demonstrated a violaceous multilobulated mass arising from the appendiceal orifice and involving the cecum. Immunohistochemical stains from both the inguinal lymph node and colonic mass were both positive for Kaposi's sarcoma and human herpesvirus-8 (HHV-8). The patient continued his HAART, and was started on doxorubicin with overall improvement in his lymphadenopathy. Castleman's disease is a lymphoproliferative disorder that has been linked to infection with HHV-8, and has also been associated with HIV, lymphoma, POEMS (polyneuropathy, organomegaly, endocrinopathy, M protein, and skin changes) syndrome, paraneoplastic pemphigus, and plasma cell dyscrasias. This case highlights the polymorphic clinical and radiological features of multicenteric Castleman's disease and should be considered as part of our differential diagnosis secondary to the increasing prevalence in HIV-infected individuals.

Coronary angioplasty of left main coronary artery in patient with Takayasu's arteritis

Dear Editor We are here with presenting our recent experience with left main coronary angioplasty in a young girl with Takayasu' arteritis. A 15-year-old female, without exposure to traditional risk factors for coronary artery disease, was hospitalized with recurrent chest pain at rest for the previous seven days. There was associated generalized weakness and malaise for the last three months. Physical examination was unremarkable except absence of right brachial and radial pulses. Electrocardiogram (ECG) showed 3 mm ST segment depression in the anterior precordial and inferior leads. The TropT test was positive and CPK-MB was raised. Routine biochemical and hematological investigations were normal except presence of mild normochromic normocytic anemia and raised ESR (40 mm in first hour). Serologic tests were negative for both C-reactive protein and syphilis. Indices of collagen disorders were negative. CT angiography revealed normal arch vessels, renal arteries and aorto-iiliac systems, but right axillary and brachial vessels showed diffuse narrowing. Coronary angiography revealed 90% stenosis of ostium of left main coronary artery (LMCA) and normal left anterior descending (LAD), left circumflex (LCx) and right coronary (RCA) arteries (Fig. 1). After discussing the option of CABG and coronary angioplasty (PTCA), the patient refused surgery and opted for PTCA. She underwent PTCA and stenting of LMCA (Fig. 2) with 3.5 × 12 Zotarolimus eluting stent (Endeavor® Drug-Eluting Coronary Stent, Medtronic). The procedure was uneventful and she was advised dual antiplatelet therapy (DAPT) with aspirin and clopidogrel along with oral corticosteroid. After one year of intervention she underwent CT-coronary angiography which showed patent stent in LMCA. The patient is asymptomatic in four year follow-up. Fig. 1 LAO and RAO caudal views showing stenosis of left main coronary ostium (selective engagement not done to avoid pressure damping). Fig. 2 Coronary stent placement (A) and final result (B). Takayasu's arteritis (TA), which predominantly involves the aorta and its major branches, can affect coronary artery in 9–12% of cases.1 Although rare, isolated coronary arterial involvement with normal aorta and its major branches has been reported.1 Axillary artery involvement, as present in our case, is uncommon but reported.2 Besides atherosclerosis, the commonest cause, isolated coronary ostial stenoses have also been reported due to congenital anomaly and also due to syphilis, Takayasu disease and radiation exposure.1 In our case, the patient, without any atherosclerotic risk factors, presented with both coronary ostial and axillary artery involvement. The indices of collagen vascular diseases and syphilis were negative. So TA was considered as the most probable etiology. Although CABG has been considered the “gold standard” for unprotected left main atherosclerotic disease revascularization, results of CABG have not been satisfactory in patients with TA. Though internal mammary artery (IMA) graft has excellent patency rate in atherosclerotic CAD, there is substantial risk of progressive subclavian artery stenosis in patients with TA.3,4 Besides a low patency rate, SVG graft has the added disadvantage of occlusion and aneurysm formation at the proximal anastomotic site since arterial inflammation is persistent in over 40% of cases even after treatment.5 Thickened aortic wall makes it difficult to create aortotomy incision.5 More recently PCI has emerged as a possible alternative mode of revascularization in carefully selected patients especially in those with left main ostium or trunk disease. It has been shown that the stenotic lesions of aorta and its major branches can be satisfactorily treated with angioplasty and stenting.6 There are few reports of PTCA with or without stenting in symptomatic coronary artery disease with TA (Table 1). However, data regarding long term results are limited because of paucity of cases. However, drug eluting stent (DES) can reduce the restenosis by inhibiting the proliferation of inflammatory and smooth muscle cells. Table 1 Coronary angioplasty data in patients with Takayasu's arteritis (TA). As in our case, isolated coronary ostial and axillary artery involvement is a rare presenting feature of TA.1,2 Acute success along with evident long term patency of stent in our case suggests that angioplasty and DES implantation will be an effective alternative method to CABG for coronary artery stenosis in Takayasu's arteritis.

To stent or not to stent - a challenging decision in a rare condition

Introduction: In this case we discuss the management of a patient with recurrent acute coronary syndrome due to Takayasu arteritis (TA). Case report description: In 2007, a 13-year-old Caucasian male with angina, electrocardiographic and troponin abnormalities consistent with an acute coronary syndrome, and widespread bruits, was found to have multiple arterial stenoses involving the aorta, renal and carotid arteries. The erythrocyte sedimentation rate was 32mm (0-7), C reactive protein 36 mg/L (0-7) with a mild normocytic anaemia. Coronary angiography showed triple vessel disease and he was diagnosed with TA with coronary artery involvement. Coronary artery bypass graft surgery (free left internal mammary graft to the left anterior descending artery and sequential saphenous vein graft to the intermediate and left posterolateral vessels) was performed. The patient received intensive medical therapy and angioplasty for hypertension due to bilateral renal artery stenosis. His condition continued to progress and angina recurred in 2012 with coronary angiography demonstrating occlusion of the vein graft segment to the posterolateral artery. The patient was managed medically but was diagnosed with a non-ST elevation myocardial infarction in 2013 due to occlusion of the vein graft to the intermediate. He suffered ongoing symptoms of cardiac ischaemia and after discussion with the Cardiosurgical team a decision was made to treat the diseased native right coronary artery by percutaneous coronary artery intervention (PCI) with drug eluting stents. Despite this measure the patient has experienced ongoing angina and further PCI to the ungrafted left coronary artery territories is under consideration. Discussion: TA most commonly presents in 20-30 year-old females of East Asian descent and coronary artery involvement in children is very rare. From a cardiac perspective this case highlights the challenge of managing coronary artery disease in the setting of active large vessel vasculitis. Limited data exist to guide clinicians in this setting. Whether redo cardiac surgery at age 18 would be superior to a percutaneous approach is unclear. Implications to clinical practice: 1. Our case highlights the importance of considering vasculitis in the differential diagnosis of a young patient presenting with chest pain. 2. Rare clinical scenarios can pose a management dilemma for the treating physician due to the paucity of supporting research available to direct the decision making process. Treatment strategies should be decided on a case-by-case basis and consensus opinion from the multidisciplinary team is recommended.

Accelerated destruction of erythrocytes in Tie2 promoter-driven STAT3 conditional knockout mice

AimsSTAT3 is a key modulator of activation and differentiation of macrophages. But it is still unknown if deficiency of STAT3 activates macrophages to destroy erythrocytes by phagocytosis. We generated STAT3 conditional knockout mice by crossing floxed STAT3 mice with Tie2 promoter-driven Cre-recombinase transgenic mice and clarified that Stat3 plays a critical role in the formation and activation of macrophages. Main methodsBlood cell count, reticulocyte count, serum lactate dehydrogenase, erythropoietin, iron and ferritin concentration, and life span of the erythrocytes in Tie2 promoter-driven STAT3 conditional knockout mice were analyzed. To explore the erythropoietic function of the mice, we subjected them to brief hemolytic anemia by injecting them intraperitoneally with phenylhydrazine. The fragility of erythrocytes was examined by scanning electron microscopy and osmotic tolerance test. Key findingsThe conditional knockout mice had mild normocytic anemia. They also displayed higher lactate dehydrogenase, ferritin and erythropoietin concentration, higher reticulocyte count, and a shorter lifespan of erythrocytes compared with wild-type controls. These data suggest that destruction of erythrocytes and secondary blood formation were accelerated in the STAT3 conditional knockout mice. It didn't appear due to the fragility of erythrocytes. A few of the conditional knockout mice suddenly developed acute severe anemia, high body temperature and massive splenomegaly, and died within 2weeks after the onset of anemia. SignificanceThis study provided evidence that STAT3 have a critical role in the destruction of erythrocytes by resident macrophages in the spleen.

An 80-Year-Old Woman With Left-Sided Headache and Diplopia

An 80-year-old white woman with a history of hyperthyroidism treated with radioactive iodine ablation, gastroesophageal reflux disease complicated by Barrett esophagus, osteoarthritis, breast cancer status post-bilateral mastectomy, and diverticulosis presented with severe left-sided headache and diplopia. Three weeks prior to presentation, she developed a sharp pain located over the left temporal, parietal, and occipital regions. It was associated with exquisite scalp tenderness. Over the next few days, the pain progressed, involving the left side of the face, including the periorbital region. There was no radiation of the pain, and she had little relief with over-the-counter acetaminophen. She also experienced earache, sore throat, and left jaw pain with mastication. The patient saw a dentist for these symptoms, and she was diagnosed with temporomandibular joint disorder. She was prescribed a mouth guard; however, despite its use, her symptoms progressed to a point where she was unable to open her mouth at times, and her jaw felt swollen. Diplopia started 4 days prior to presentation. She experienced this intermittently for 24 hours before it became constant. She saw an ophthalmologist who diagnosed her with a right eye abduction deficit presumed to be a cranial nerve 6 (CN6) palsy. The patient then went to the emergency department for further evaluation. Review of systems was notable for fatigue, recent 10-pound weight loss, and intermittent myalgias, but there were no fevers, chills, dizziness, dysphagia, dysarthria, weakness, or numbness. Family history included coronary artery disease, diabetes, and various cancers. She was a 40-pack-year smoker, but quit 12 years ago. Her general physical examination was only notable for a blood pressure of 164/77 mm Hg. Neurological examination was notable for the inability to fully abduct the right eye. Fundoscopic examination was negative for papilledema. Strength was 5/5 throughout with normal tone. Serum laboratory analysis showed mild leukocytosis (12 200/mm3), normocytic anemia (hematocrit of 32.9% and mean corpuscular volume of 80.6 fL compared to hematocrit 40.2% 2 months prior), and thrombocytosis (675 000/mm3). Erythrocyte sedimentation rate (ESR) was 76 mm/h (reference range 0-30) and C-reactive protein (CRP) was 73.65 mg/L (reference range 0.30-8.00). A lumbar puncture (LP) was performed with a normal opening pressure of 15 cm H2O. The white blood cell count was 1 in tube 1 and 2 in tube 4. The red blood cell count was 9 in tube 1 and 1 in tube 4. The glucose was slightly elevated at 79 mg/dL (reference range 40-70), and the protein was normal at 41 mg/dL. The viral and bacterial studies of the cerebrospinal fluid (CSF) were unremarkable. Magnetic resonance imaging (MRI) of the brain and orbits with and without contrast was unremarkable except for moderate supratentorial white matter changes. Magnetic resonance angiogram of the head and neck with and without contrast was normal.

Early cutaneous metastasis from colonic adenocarcinoma

CASE REPORT A 74­year­old female presented acutely to the surgical department with two rapidly growing, painful skin lumps. Her medical history included an emergency right hemicolectomy for perforated transverse colon secondary to a Dukes’ C1 T4 N1 M0 poorly differentiated colonic adenocarcinoma one month previously. Physical examination revealed a tender 3 cm cervical nodule (Figure 1) and a 2 cm nodule in left iliac fossa at the previous drain site (Figure 2). Laboratory testing revealed a mild normocytic anaemia (hemoglobin 10.4 g/L) and acutely deranged liver function tests. Computed tomograpy scan of the neck, chest, abdomen and pelvis confirmed a 3x3 cm necrotic left supraclavicular lymph node, 2.8x1.9 cm abdominal wall nodule in the left iliac fossa, and mild ascites. Fine needle aspiration cytology established a diagnosis of poorly differentiated metastatic adenocarcinoma. This patient was not a candidate for chemotherapy and she was treated with palliative care. DISCUSSION Cutaneous metastasis from colonic cancer is rare with an incidence of around 4% [1] and only a few cases have been reported [2–4]. Cutaneous metastasis may present at a variety of sites such as the abdominal wall, CLINICAL IMAGES OPEN ACCESS

Polymicrobial endocarditis involving Veillonella parvula in an intravenous drug user: case report and literature review of Veillonella endocarditis

Veillonella spp. are strictly anaerobic, Gram-negative cocci able to ferment various substrates (pyruvate and lactate) that usually present as commensals in the oral, gastrointestinal, and female genital tract microflora [1]. This genus has been reported to be pathogenically involved in periodontitis, periodontal abscess, and various acute oral conditions. In addition, Veillonella spp. may be exceptionally involved in severe infections, including meningitis, osteomyelitis, or prosthetic joint infection [2]. Infective endocarditis (IE) constitutes one of the most serious, albeit uncommon, complications of bloodstream infection (BSI) by Veillonella spp. in patients with predisposing conditions such as valvular heart disease or intravenous (IV) drug abuse [3]. Here we describe a case of IE due to V. parvula in an IV drug user (IDU) and review the scarce literature on this entity. A 35-year-old man presented to the Emergency Department (ED) of our hospital with fever, chills, purulent sputum, and pleuritic pain for about 48 h. He was a current smoker (index of 20 pack-years) and acknowledged a history of active IV drug abuse (heroine and cocaine). His temperature was 39 C, blood pressure was 120/70 mmHg, and his respiratory rate was 24 breaths per minute (bpm). Physical examination revealed a poor oral hygiene with periodontal disease, venipuncture marks in the upper extremities, and basal crackles over the right lung, with no audible cardiac murmurs. Laboratory data showed a mild normocytic anemia (hemoglobin 11.3 g/dL) and white cell count (WCC) of 9.8 9 10/L. A chest X-ray was unremarkable. Because of our clinical suspicion of IE, we initiated empiric treatment with IV ceftriaxone, cloxacillin, and gentamicin. A transthoracic echocardiography (TTE) revealed two oscillating masses (1.5 9 0.5 and 1.5 9 0.4 cm, respectively) on the tricuspid valve with mild regurgitation, and a thoracic computed tomography (CT) showed multiple cavitating nodules compatible with pulmonary septic embolisms. Viridans group Streptococcus was identified by the semiautomated WIDER system (Francisco Soria Melguizo S.A., Madrid, Spain) in four out of four aerobic bottles of blood cultures (BCs) taken at admission and processed using the BacT/Alert System (bioMerieux, Marcy l’Etoile, France). The isolate was not identified to species and was sensitive to penicillin, cefotaxime, ceftriaxone, erythromycin, clindamycin, levofloxacin, trimethoprim–sulfamethoxazole, and vancomycin; therefore, treatment with cloxacillin was discontinued. The patient initially became afebrile, but after 14 days of treatment with ceftriaxone and gentamicin persistent daily fever reappeared. Before the results of repeated BCs were available, the patient had left the hospital ward without medical authorization. He returned 3 days later to the ED complaining of fever (38.8 C) and left pleuritic chest pain a few hours after an IV heroin injection. He was hemodynamically stable, and tachypneic (18 bpm), and the abdominal examination was remarkable for the identification of a 2-cm tender hepatomegaly and 4-cm splenomegaly that had not been noted on the previous admission. The WCC M. A. Perez-Jacoiste Asin I. Serrano-Navarro S. Prieto-Rodriguez Department of Internal Medicine, University Hospital ‘‘12 de Octubre’’, Instituto de Investigacion Hospital ‘‘12 de Octubre’’ (i?12), Universidad Complutense, Madrid, Spain

Leptospirosis Diagnostic Challenges, American Samoa

Leptospirosis Diagnostic Challenges, American Samoa

Bilateral foveal cysts secondary to Streptococcus constellatus endocarditis

Infective endocarditis can be acute or subacute, depending on the virulence of the causative organism. It can also cause loss of vision by a variety of mechanisms, ranging from embolic retinal artery occlusion to endogenous endophthalmitis. We illustrate the first report of foveal cyst formation secondary to infective endocarditis. A 53-year-old man presented to his general practitioner with a variety of constitutional symptoms, but initial laboratory and imaging investigations revealed only mild normocytic anaemia, and he was discharged from further medical care. Four weeks later he developed bilateral visual loss associated with whitish lesions of the superficial retina at both foveae. These later developed into foveal cysts with disruption of the photoreceptor inner segment-outer segment junction and persistent poor visual acuity of 6/60 OU. No retinal haemorrhages or Roth spots were noted. Only after he presented with visual loss did further investigations reveal the underlying diagnosis of streptococcal endocarditis. Ophthalmologists assessing retinal pathology which presents in association with undiagnosed constitutional symptoms are advised to refer such patients promptly for thorough medical investigation, including blood culture and echocardiography where appropriate.

Familial Amyloidotic Polyneuropathy with Diffuse GI Involvement

Purpose: Amyloidosis is a disease associated with multiorgan deposit of insoluble proteins that are resistant to proteolytic degradation. GI tract involvement can result in esophageal dysmotitlity, abdominal pain, chronic diarrhea with malabsorption, perforation and bleeding. GI involvement can occur with all types of amyloidosis including the rare autosomal dominant hereditary forms. The most common hereditary form is the Familial Amyloidotic Polyneuropathy also known as transthyretin amyloidosis (ATTR). A 37-yr old male presented with a 1-yr history of intermittent postprandial epigastric pain and watery non-bloody diarrhea with tingling and numbness in his fingers and toes, dizziness while standing up and 40 lb weight loss. His two brothers had similar complaints. He appeared emaciated and had orthostatic changes that did not respond to IVF hydration. His abdomen was soft with mild epigastric tenderness and mild hepatomegaly. He had a mild normocytic anemia with normal ferritin, vitamin B12 and folate; albumin was normal. HIV and stool studies were negative. EGD was normal. Duodenal biopsies revealed eosinophilic material with apple green birefringence under polarized light on Congo red stain typical for amyloid. Colonoscopy was normal and biopsies showed amyloid in the colon and ileum. The samples were sent for liquid chromatography-mass spectrometry and revealed transthyretin type amyloid deposits. ATTR is caused by a mutation in the transthyretin gene that leads to the production of an altered transthyretin protein by the liver. This altered protein deposits predominately in the peripheral and autonomic nerves manifesting as paresthesias and orthostasis. It can also affect the gut, the heart and the kidneys. It is a universally fatal disease. The only established therapy is orthotopic liver transplantation. Our patient is being referred for OLT evaluation pending a medical card. He has received moderate improvement in diarrhea with loperamide and with short courses of antibiotics for possible underlying bacterial overgrowth. Fat soluble vitamins are being supplemented. Gabapentin and midodrine have been used with good response for his paresthesias and orthostasis, respectively. Amyloid deposition in the GI tract is an uncommon finding during work-up of a patient with chronic diarrhea. Most of these patients develop amyloid in response to plasma cell dyscrasias or chronic inflammation and its main treatment is that of the primary disease. The combination of amyloid deposition with peripheral neuropathy should alert the clinician to suspect this rare multisystemic hereditary disease since it is fatal and it can be potentially treated with OLT.

The Case Files

A 62-year-old woman with a past medical history of breast cancer presented to the emergency department with three weeks of intermittent left scapula pain. The onset was at rest, and she had no history of trauma. The pain was not made worse or relieved by change in position. She denied any associated symptoms, but a review of systems revealed a few episodes of abdominal fullness over the preceding three weeks. She denied chest pain, shortness of breath, abdominal pain, nausea, vomiting, diarrhea, fever, chills, leg pain or swelling, and recent travel. Prior treatment for the pain included over-the-counter analgesics, which offered minimal relief. She had outpatient evaluations by a cardiologist and a neurologist for her shoulder pain before her ED visit. The outpatient doctors ordered numerous blood tests, a transesophageal echocardiogram (TEE), and an MRI of the lumbosacral spine. The indications for these diagnostic modalities were unknown to the patient. The TEE was unremarkable, and MRI showed a clinically insignificant lumbar disc herniation. The patient had bilateral lumpectomies in 2000 and 2002, and additional past medical history included palpitations and mitral valve prolapse. She denied tobacco, alcohol, or drug abuse. The patient's vital signs on arrival in the ED were unremarkable. She was uncomfortable, her abdominal exam included normal bowel sounds, and her abdomen was flat, not obese, not distended, and nontender without palpable organomegaly. A back exam revealed no tenderness to palpation and no deformity. The remainder of her physical exam was normal. The patient received ketorolac, oxycodone/acetaminophen, and diazepam. Blood work was drawn, and a CT of the chest with contrast to rule out PE was obtained. The labs were unremarkable except for a mild normocytic anemia. The CT of the chest was extended to the abdomen during the exam at the order of the attending doctor when the CT technologist recognized a suspicious mass on the last cuts of the CT chest. The abdominal CT revealed a large abdominal mass measuring 13 cm x 15 cm x 24 cm in size, encasing and displacing the abdominal aorta, inferior vena cava, and the left kidney, while extending from the left diaphragmatic crus to the left iliac fossa. The patient was admitted, and underwent percutaneous biopsy. The pathology was consistent with lymphoma. The patient was subsequently discharged home with oncology follow-up as an outpatient. She is now awaiting a specialized multifaceted treatment plan from her surgeon and oncologist.ImageReferred pain is found in the literature as early as 1893 when Sir Henry Head, an English neurologist, included the phrase “referred tenderness and pain” in his paper, “On Disturbances of Sensation with Especial Reference to the Pain of Visceral Disease.” (Brain 1893;16:1.) Since then, it has been defined as pain perceived at a site adjacent to or at a distance from the site of origin. (Clin J Pain 2001;17[1]:11.) Several neuroanatomical and physiological theories focus on this concept. Collective conclusions from past studies state that nociceptive dorsal horn and brainstem neurons receive convergent inputs from various tissues; therefore, higher centers cannot identify the actual input source correctly. The best known example is pain experienced during a heart attack. Nerves from damaged heart tissue convey pain signals to spinal cord levels T1-T4 on the left side, which are the same levels that receive sensation from the left side of the chest and part of the left arm. Another example involves pain from a ruptured spleen or splenic abscess. Called Kehr's sign, it is the referred pain from abnormal spleen pathology irritating the diaphragm. The sensory fibers of one of the phrenic nerves send pain signals to the spinal cord at C3-C5. Neurons at these spinal cord levels also receive sensation from the shoulders via the supraclavicular nerves. The patient in this case was experiencing referred pain from the large abdominal mass abutting the diaphragm, causing signals to be sent via the phrenic nerve to the brain and making the patient perceive the pain as coming from the shoulder. Unfortunately, the mass was not able to be palpated by physicians due to its posterior location in the abdomen nor was it readily distinguishable from the other abdominal organs because of the mass spanning across the entire abdomen from the diaphragm to the bony pelvis, making it critical to obtain a CT of the abdomen and pelvis. It is important for physicians to remember the concept of referred pain when diagnosing and treating presumed musculoskeletal complaints, especially in instances when extensive diagnostic testing has elicited no cause. Had the symptom been considered before her ED visit, it may have led to the correct diagnosis and earlier intervention.

Monocular Vision Loss and Headache in a 60-Year-Old Liver Transplant Patient

Monocular Vision Loss and Headache in a 60-Year-Old Liver Transplant Patient

Pulmonary hypertension associated with Ehrlichia canis infection in a dog

CANINE monocytic ehrlichiosis (CME) is an important canine disease with a worldwide distribution. The clinical presentation can be acute, subclinical or chronic, and there may be a multitude of clinical...

Isolated motor conduction block associated with infliximab

TNF-alpha antagonists have been associated with various types of peripheral neuropathies, including multifocal motor neuropathy with conduction block and mononeuropathies [1]. We present two patients treated with infliximab who developed unifocal motor neuropathy with conduction block. A 34-year-old female with Crohn’s disease developed painless weakness of right-hand pincer grip of insidious onset. She had previously received five courses of infliximab infusions (5 mg/kg) and a further dose 3 days after symptom onset. Infliximab partially controlled gastrointestinal symptoms and she was otherwise well. Regular medication included the oral contraceptive pill, levothyroxine, folate, omeprazole, B12 injections, and iron infusions. Examination revealed MRC grade 4 power of the right abductor pollicis brevis, flexor pollicis longus, flexor digitorum profundus (median), and opponens pollicis. Flexor carpi radialis was mildly weak (4?) but forearm pronation remained strong. There were no sensory signs and systemic examination was unremarkable. A detailed four-limb neurophysiological examination 6 weeks after symptom onset revealed isolated severe right median motor conduction block 2.5–6.5 cm proximal to the antecubital fossa skin crease (Fig. 1). Median and other sensory conduction responses were normal. EMG of median innervated forearm muscles including abductor pollicis brevis and flexor pollicis longus was consistent with conduction block, with reduced recruitment of motor units but no spontaneous activity or other evidence of motor axon loss. Right median sympathetic skin response, somatosensory evoked potentials, and thenar thermal threshold testing were all normal. There was evidence for systemic active inflammation with mild leukocytosis, thrombocytosis, and normocytic anemia; ESR 102 mm/h and CRP 51 mg/l. Anti-DNA antibodies, ANCA, ANA, RA latex, glycolipid and antiGAD antibodies, anti-GM1, and anti-GQ1b antibodies were either normal or negative. An MRI with gadolinium showed hyperintensity of the right median nerve in the lower third of the right arm on TIRM and T2-weighted images, with subtle enhancement but no enlargement. This corresponded to the site of conduction block. No specific treatment was given, but there was significant improvement of power in weak muscles within 4 weeks of presentation, and complete recovery at 1 year. Patient 2, a 41-year-old female with ankylosing spondylitis, had been treated with regular infliximab infusions since 2003. In April 2009, she awoke with painless weakness of left finger and wrist extension 3 days after an infliximab infusion (270 mg). Examination revealed MRC grade 0 finger extension and 4wrist extension with radial deviation and no sensory loss. Initial neurophysiological examination 1 week after symptom onset showed profound A. W. Michell (&) Department of Clinical Neurophysiology, Box 124 Addenbrooke’s Hospital, Cambridge CB2 0QQ, UK e-mail: andrew.michell@addenbrookes.nhs.uk

Massive Colonic Intussusception Demonstrated on CT When Abdominal X-ray Suggested Sigmoid Volvulus

Purpose: Describe a case of colonic intussusception with colon cancer as a lead point discovered on CT when initial abdominal film was suggestive of sigmoid volvulus. Case: A 36-year old male was referred for evaluation of chronic left lower quadrant abdominal pain with associated alteration in bowel movements and 35 pound weight loss over 3 to 4 months. Routine blood work revealed a mild normocytic anemia. Colonoscopy revealed a large ulcerating 8cm x 5cm splenic flexure mass. Two days later, he presented to the emergency room with worsening left lower quadrant abdominal pain with passage of bloody mucus, but no flatus or stool. An abdominal x-ray showed dilated loops of colon in the right hemi-abdomen, but a sigmoid volvulus could not be ruled out. A CT scan revealed a complete bowel obstruction due to a very large descending colon intussusception with the splenic flexure mass serving as a lead point and a portion of the stomach invaginating inferiorly into this intussusception. He had emergency surgery with en bloc colon resection, diverting transverse colostomy, and long Hartmann's pouch. Final pathology revealed a T3 N0 lowgrade adenocarcinoma. Conclusion: Intussusception is rare in adults and is usually due to larger polyps or tumors. This case illustrates the need to pursue further imaging with CT when there are questionable abnormalities on plain abdominal x-ray. Abdominal CT is the most sensitive imaging exam for the diagnosis of intussusception and allows for the detection of a lead point.Figure: No Caption available.Figure: No Caption available.

Web of Confusion

c t p m ( PRESENTATION The occurrence of a late-stage complication in a patient with early disease, reminds us that any illness can take an unpredictable course. A 63-year-old man presented with complaints of fatigue and rash. He had been in his usual state of health until approximately 2 months prior, when he developed decreased visual acuity in his right eye. He was seen by a local ophthalmologist, who diagnosed nonarteritic ischemic optic neuritis and prescribed a daily aspirin. Soon thereafter, the patient noticed that he was having trouble moving about his house and working, and he felt as if he needed to sit and rest often. Additionally, he admitted to night sweats and a 15-lb weight loss. Upon questioning, he also reported that he had developed a nonpruritic rash on his legs and torso. He denied headache, joint pain, myalgia, morning stiffness, jaw claudication, weakness, cough, or shortness of breath. He took no medications other than a daily adult aspirin. On examination, the patient exhibited livedo reticularis involving his lower limbs, buttocks, and lower torso circumferentially (Figures 1 and 2). He was normotensive, afebrile, and had no other rash, nodules or ulcers. His joints were normal, as were his heart, lungs, and abdomen. Peripheral pulses were present, and his temporal arteries appeared normal and were nontender.

Fevers, headache and abnormal liver function in a 68-year-old man

A 68-year-old man was transferred to our unit from a local hospital for further investigation of pyrexia of unknown origin (PUO). He had consulted his GP intermittently over the previous two years with non-specific aches and pains, and mild fatigue. Two weeks prior to admission he noticed low back pain followed by high fevers, chills, nausea and diarrhoea. Past medical history included a nephrectomy for renal cell carcinoma and ischaemic heart disease. He was born in Kenya, but had been resident in the UK for 30 years, and was married with three children. He had never smoked and drank minimal alcohol. Two months prior to admission he had travelled to Kenya for a holiday, and had not taken anti-malarial prophylaxis. On presentation to our unit the patient was haemodynamically stable, with a temperature of 36.8°C. There was no lymphadenopathy or organomegaly, and there were no skin changes. Examination of the cardiovascular, respiratory, and neurological systems was unremarkable. Initial blood parameters demonstrated a mild normocytic anaemia (Hb 10.4 g/dL, MCV 85.8 fl), moderate renal impairment (urea 13.6 mmol/L, creatinine 234 mmol/L), significantly raised inflammatory markers (ESR 80 mm/hr, CRP 179 mg/L), and abnormal liver function (albumin 26 g/L, PT 14.5 s, ALT 47 U/L, ALP 715 U/L, GGT 300 U/L). Three thick and thin blood films were negative for malarial parasites as were multiple cultures of blood, stool and urine. A CT scan of the whole body was normal. Viral hepatitis, HIV and autoimmune serology were negative. Over subsequent days low-grade fevers were noted, and the patient complained of mild intermittent headaches. Renal function improved with increased oral fluid intake, but liver function continued to deteriorate (albumin 16 g/L, PT 15.3 s, ALT 338 U/L, ALP 1071 U/L, GGT 496 U/L). An ultrasound scan of the liver and biliary system was normal. A percutaneous liver biopsy revealed granulomatous arteritis with prominent giant cell involvement (Figure 1). No acid-fast bacilli were identified. Prompted by this unexpected finding, a temporal artery biopsy was undertaken which confirmed patchy granulomatous inflammation with giant cell involvement. A final diagnosis of giant cell arteritis (GCA) was, therefore, made and treatment with high-dose oral prednisolone was initiated. His symptoms improved rapidly, and he was discharged shortly afterwards on a tapering prednisolone regimen. Liver function has since normalized.