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Khaled N. Almusrea, MBBS, FRCSC
Observation of rumen movement at the left sublumbar fossa is only possible in good light and in animals that have a short coat cholesterol ranges normal buy zocor 10 mg on-line. The moving rumen can be detected indirectly by observing the lateral displacement of the body wall cholesterol and eggs myths quality zocor 20 mg. Palpation of the rumen is achieved by exerting pressure on the rumenal wall via the left sublumbar fossa using a clenched fist cholesterol guidelines calculator purchase 40 mg zocor otc. As the wave of movement passes beneath the hand the hand can be felt to be pushed gently outwards cholesterol kit cvs purchase zocor 5 mg on line. Auscultation of the rumen movements by stethoscope is the most sensitive of the three methods cholesterol levels natural remedies 5mg zocor fast delivery. The phonendoscope diaphragm is placed in the sublumbar fossa and directed downwards towards the rumen cholesterol chinese food order 5 mg zocor free shipping. Using this method, weak contractions can be detected that may be missed by the other techniques. Percussion of the left abdominal wall will produce resonance over the gas in the dorsal sac of the rumen. As the percussion proceeds ventrally the resonance declines over the fibre and fluid sectors of the rumen. Differentiation of the A and B waves can only reliably be made by detecting eructation. This can be done by observation, listening or by auscultation with a stethoscope over the trachea. Auscultation of reticular contractions can sometimes be achieved by stethoscope auscultation over ribs 6 or 7 ventrally on the left side. A diphasic contraction every 40 to 60 seconds at the start of the A cycle can 88 sometimes be detected. Palpation of the left abdominal wall may enable pain to be localised, although reactions by fractious animals may be misleading. Pneumoperitoneum caused by intraperitoneal gas may cause mild distension of the right and left sublumbar fossae. Pneumoperitoneum is usually less tympanic, and the normal rumen can be palpated through the left sublumbar fossa. A diagnosis of ruminal bloat can be supported if hyper-resonance is present on percussion of the distended left sublumbar fossa. Differentiation between frothy and free gas bloat can only be achieved by attempts at decompression. In cases of ruminal acidosis, the fluid volume of the rumen will increase due to osmosis into the hypertonic rumen. Rumen fluid collection and analysis when pyloric obstruction, ruminal acidosis or poor rumen function are suspected may provide useful additional information. There are several tests and signs that may support a diagnosis of traumatic reticulitis. Animals that have progressed to a traumatic reticulopericarditis may have additional cardiovascular signs, including signs of congestive heart failure. The animal may grunt when it moves or breathes due to pain induced by parietal peritoneal irritation. The detection of a grunt is improved by auscultation with a stethoscope placed against the trachea. Acondition should not be ruled out if a grunt is absent, but if a grunt is present this indicates there is anterior abdominal pain. The animal is reluctant to move, has an arched back and grunts while defaecating with a raised tail. If there is a penetrating foreign body which Clinical Examination of the Gastrointestinal System Figure 8. The bar test and the knee test involve upward pressure on the xiphoid area to check for discomfort and associated grunting. A padded metal or wooden bar is placed beneath the animal and positioned just behind the xiphisternum. The veterinary surgeon should place a stethoscope over the trachea in the ventral midline of the neck and auscultate for a grunt. In an animal with an acute traumatic reticulitis this sudden movement will often elicit discomfort and a grunt. Localisation of the pain can sometimes be achieved by regional palpation or percussion of the anterior abdomen. A stethoscope is placed over the trachea and a hand placed in the left sublumbar fossa to detect ruminal movement. A quiet and otherwise ordinarily inaudible grunt may be heard via the stethoscope just before the commencement of the ruminal component of the A wave. The grunt is caused by the pain elicited by the double reticular contraction causing the penetrating foreign body to produce parietal peritoneal irritation. Further investigations which may be useful include sampling of the peritoneal fluid by peritoneal tapping, radiography, examination using a metal detector and laparotomy/rumenotomy. Acompass can be used to indicate the presence of a prophylactic magnet in the reticulum. If a magnet is found to be present, indicated by the movement of the compass needle, traumatic reticulitis is less likely to be the cause of the illness. No physical examination of the left side of the body is complete without checking for a left displaced abomasum (Figs 8. Left displacement of the abomasum is a very common condition in high yielding dairy cows and is usually recognised during the first few weeks after calving. Rothera tablets or the ketone patch on a urine test stick can be used to confirm the presence of ketones. The presence of a left displaced abomasum must always be checked for during the examination of the abdomen of adult cattle. In this condition the fluid and gas filled displaced abomasum is between the left abdominal wall and the rumen. The musical tinkling sounds produced by escaping gas bubbles can sometimes be heard by simple auscultation using a stethoscope and are probably produced in response to adjacent ruminal movements. Alternatively, gentle ballottement of the abdomen using a clenched fist or by gentle rocking may evoke them. High pitched resonant pings can be produced by percussion of the displaced abomasum. The pings may be heard in association with the musical tinkling sounds of escaping gas by simultaneous auscultation using a stethoscope. The ping sounds like a basketball being bounced upon a concrete floor or a steel drum being hit. It is suggested that clinical evaluation should be focused along a line drawn from the left elbow to the left tuber coxae, although it can be found much higher or lower than this. In general, clinical evaluation from the 9th to the 13th rib along this line is often the most rewarding. This can usually be discounted by Clinical Examination of the Gastrointestinal System Abomasum Rumen Left Right Omasum Figure 8. To perform an abomasocentesis, the skin in the intercostal space over the ping is antiseptically prepared and a lumbar-spinal needle quickly inserted. If the pH is between 2 and 4 this usually confirms the diagnosis if the clinical presentation is consistent. If it is impossible to obtain a fluid sample, a section of damp pH paper can be held close to the hub of the needle in the stream of escaping gas from the abomasum. Ultrasonography can be used to identify the displaced abomasum as the folds of the abomasal mucosa contrast with the papilliform mucosa of the rumen. Alternatively, if the abomasum can be identified by ultrasonography in the normal position just to the right of the ventral midline, a diagnosis of left displaced abomasum can be ruled out. Laparoscopy or surgical laparotomy will allow direct visualisation to rule in or rule out a left displaced abomasum. Examination of the right side of the abdomen Examination of the right side of the abdomen is performed to assess the gravid uterus, the abomasum, the intestines and the liver. Abomasum, intestines and the gravid uterus Abnormal contours identified earlier should be explored in more detail. Distension of the right sublumbar fossa may be seen with right-sided abomasal or caecal dilatation and/or torsion. Other causes include distension of the rumen in vagal indigestion, omasal impaction and abomasal impaction. The technique of simultaneous percussion and auscultation is used to explore the right side of the body. Pings produced by percussion and auscultation represent abnormal accumulations of fluid and gas within abdominal structures. The right body wall should be examined by percussion and auscultation dorsal and ventral of a line from the elbow to the tubae coxae. Conditions producing pings include abomasal dilatation, caecal dilatation or torsion, gas in the rectum and pneumoperitoneum. Normal intestinal sounds called borborygmi can be heard intermittently in the right ventral quadrant; these normally occur every 15 to 30 seconds but may be inaudible. Splashing sounds caused by excessive fluid in the intestines may be detected by ballottement and succussion. These sounds may be detected in association with an enteritis, ruminal acidosis or intestinal obstruction. Ultrasonography of the small intestines is possible, and peristaltic movements can be observed easily in the normal animal. Ballottement of the lower flank in late pregnancy will cause the foetus to impact on rebound on the ballotting hand. Sometimes large lumps of fat present in fat necrosis and impactions of the abomasum may also be detected in this way. Pain tests should be performed on the anterior ventral quadrant of the abdomen by pressing the knee or a clenched fist quickly and firmly into the abdomen. A sharp pain may indicate a focal peritonitis secondary to a perforated abomasal ulcer. Additional techniques include radiography, laparoscopy, exploratory laparotomy and postmortem examination. Prehepatic causes of jaundice, such as haemolytic anaemia, are more common in cattle. If it is grossly enlarged or displaced posteriorly it may be palpated by pushing the fingers behind the right costal arch. The liver may be enlarged in chronic liver fluke infestation and congestive heart failure. The risks of severe iatrogenic haemorrhage during and following this procedure must be considered. Examination of the contents of the peritoneum Detection of excessive fluid in the abdomen by physical means is difficult unless accumulations are large. The results of ballotting for a fluid thrill are difficult to interpret because of the fluid content of the ventral rumen. Transudates or urine in the peritoneum can be identified as non-echogenic fluid images. Peritoneal samples can be assessed by gross examination or sent for laboratory analysis and bacteriological culture. Ultrasonography Using ultrasonography, the size, position and consistency of the liver can be characterised and the presence of abscesses may be confirmed. The gall bladder lies on the caudal border of the liver but is seldom involved in pathology, although it may be enlarged in some cases of salmonellosis. Biochemical changes such as hypoproteinaemia occur in some types of liver disease. Conjugated bilirubin increases with bile duct obstruction and unconjugated bilirubin increases in haemolytic anaemia. Rectal Clinical Examination of the Gastrointestinal System examination is usually limited to cattle over 12 months of age and, to avoid creating a pneumorectum and tenesmus which may confuse abdominal auscultation and percussion, is the last part of the clinical examination. Rectal examination of the gastrointestinal tract can be used to detect a viscus which is displaced or enlarged. The rectal examination is particularly useful in palpating a grossly distended rumen, caecal dilatation and torsion, gut tie, and intestinal intussusception. Indicators of peritonitis such as adhesions and a sandy grating sensation may be palpable. If blood is seen on the glove, bleeding of the mucosa may be suggested and the examination should be curtailed. The rectal examination the contents of the posterior abdomen should be checked in a set order to avoid missing any organ. Each quadrant examination area is palpated and the organs present assesed or noted if unexpectedly absent. Parts of the small intestine and large intestine can be felt but are not discrete structures. In the normal animal it is possible to palpate the caudal surface of the dorsal sac of the rumen to the left of the pelvic brim. A left displaced abomasum cannot be felt per rectum unless the gas-filled viscus is displaced very high and caudal in the left flank, which is exceptional.
A careful drug history and high index of suspicion is critical in making the correct diagnosis cholesterol levels explained effective zocor 5mg. Her medical history included hypertension managed with hydralazine at stable doses for several years lowering cholesterol in diet buy 10 mg zocor with mastercard. Examination was significant for pallor cholesterol chart for males trusted zocor 20mg, labored breathing and coarse crackles on bilateral lung fields list of cholesterol lowering foods cheap zocor 20mg with visa. She was stabilized on high flow oxygen and following lab tests revealed moderate anemia (Hb-6 high cholesterol foods diet order zocor 10 mg without prescription. Computed Tomography scan of the chest without contrast revealed bilateral airspace opacities cholesterol levels of heart attack victims purchase zocor 20mg free shipping. Because of her increased oxygen requirements, steroid pulse was started to halt worsening of hypoxia. While her respiratory status improved, her creatinine worsened, and urinalysis showed hematuria and proteinuria. A kidney biopsy was recommended for evaluation of glomerulonephritis, but the patient declined. Subsequently, she was started on plasmapheresis and immunosuppressive therapy with rituximab. The patient sleeps with 2L of oxygen via nasal cannula with saline humidifier and uses fluticasone three times daily for nasal congestion. She denies personal or family history of bleeding or clotting disorders, easy bruising, or anemia. She experienced no complications or excessive perioperative bleeding during previous cholecystectomy, pregnancy, or vaginal delivery. Her pulmonary hypertension was diagnosed via echo 4 years prior, and subsequent cardiac catheterization showed a mean pulmonary arterial pressure of 43 mmHg. Physical exam demonstrated intranasal dried blood without visible vessel or abrasion. A reported 24-33% of patients with antiphospholipid antibodies are predisposed to vascular thrombosis (Gastineau et al. Recent studies demonstrated a potentially causal relationship between lupus anticoagulant and idiopathic pulmonary hypertension (Parthvi et al, 2017). The pathophysiology remains unclear, but some hypothesize it may develop due to thrombosis, chronic thromboembolism, and associated endothelial remodeling (Zuily et al. Early identification of antiphospholipid antibodies can allow physicians to appropriately screen and treat before irreversible pulmonary vascular pathology occurs. Laboratory features include low complement levels (88%), anemia, leukocytopenia or lymphocytopenia and thrombocytopenia. Imaging findings include bowel wall edema with characteristic target sign, ascites, hydronephrosis, mesenteric abnormalities and bowel dilation. Physical exam at each admission revealed a woman with dry mucus membranes, and bilateral lower abdominal tenderness. On a prior admission, the patient was treated with ciprofloxacin and metronidazole with no relief of symptoms until intravenous methylprednisolone, 20 mg every eight hours, was initiated. The patient had complete resolution of symptoms, but returned to the hospital shortly after due to recurrence. The patient also had a rash on his face about 2 weeks prior but could not describe the appearance. The patient went to urgent care and was found to be bradycardic, so he was sent to the emergency department for further evaluation. Physical exam showed bradycardia at 35 bpm, regular rhythm, normal S1 and S2, no S3 or S4, and no murmurs or rubs. Echocardiogram showed normal left ventricular systolic and diastolic function, mild aortic, mitral, and tricuspid regurgitation. Lyme carditis is a rare entity and more recent data estimates an incidence of about 1% of patients with Lyme disease. Given its rarity, physicians should be able to diagnose and treat lyme carditis, as missing the diagnosis could result in severe rhythm abnormalities leading to death. It is caused by a spirochete, Borrelia burgdorferi, transmitted by the Ixodes tick. Early manifestations are characterized by a distinctive skin lesion, known as erythema migrans. Parenteral antibiotic therapy is recommended with ceftriaxone, and in some severe cases temporary pacing may be required and indications are similar as with other cases of heart block. She was found to have left eye retinal whitening superior to the macula to which vitreous tap was performed. Patient started on empiric treatment with injection of vancomycin, ceftriaxone, and voriconazole. Empiric antibiotic with Bactrim was started to cover for Toxoplasmosis since patient had cat exposure. However, Burgdorferi IgM was 3/3 bands positive and patient was diagnosed with lyme endophthalmitis. Ophthalmology and Infectious Disease consult teams recommended ceftriaxone for 2 weeks and outpatient follow up with both specialists. Ocular Lyme remains an underdiagnosed disorder because of difficulties in serodiagnosis and because clinical ocular features can be nonspecific and vague. Often in healthy young patients, these symptoms can be attributed to more common conjunctivitis or uveitis and the diagnosis of lyme disease can be delayed and detrimental to the patient. Endophthalmitis should be high in the differential diagnosis because it can lead to not only visual loss, but also increased risk of mortality. Ocular manifestations have been reported to occur in different stages of Lyme borreliosis in early stages, within a few weeks to a few months of infection, and, in the late stage, several months to years after the infection incident. Ocular and systemic symptoms of endophthalmitis are usually nonspecific, and early diagnosis and treatment are important to prevent blindness. Physicians treating patients from lyme disease endemic areas need to be aware of the protean clinical manifestation. Systemic findings, meticulous exclusion of other infectious and detailed medical history are essential. On exam she was hypertensive, disoriented and frail without lymphadenopathy or hepatosplenomegaly. Thyroid ultrasound, sestamibi parathyroid scan, and nuclear bone scan revealed scattered lucent lesions of the calvarium and a 1. When workup is inconclusive, clinical suspicion should prompt further investigation to identify an underlying etiology. Presenting features include leukocytosis with lymphocytosis, generalized lymphadenopathy, hepatosplenomegaly, and hypercalcemia with lytic bone lesions in up to 70% of cases. This case presented a diagnostic dilemma as extensive workup did not reveal a clear underlying etiology. On exam, patient was unresponsive with Glasgow Coma Scale of 7, sluggish pupils, diffuse rigidity, brisk reflexes, and dry mucous membranes. Finger-stick glucose was 14 and mental status improved within minutes after administration of 50% dextrose (D50). Electroencephalography showed moderate diffuse neuronal dysfunction without seizures. Workup for hypoglycemia found a low plasma glucose with simultaneous high insulin level of 68. Pathology ultimately revealed an intermediate grade metastatic neuroendocrine tumor with a positive insulin stain consistent with a malignant insulinoma. Our case is an uncommon case of a metastatic insulinoma with a large primary pancreatic tumor and multiple metastatic lesions. Insulinomas secrete insulin not regulated by glucose levels thus leading to hypoglycemia. Patients may present with hypoglycemic symptoms, including headache, lethargy, seizures, altered mentation, palpitations, sweating, or tremulousness triggered by exercise or fasting and improved with eating. In our case, we surmise the changes in mental status and frequent snacking were indicative of hypoglycemia. Diagnosis of insulinoma is made with combined low blood glucose and elevated insulin, proinsulin, and Cpeptide levels. Imaging or angiography with pancreatic venous sampling confirms and localizes the tumor. Our case is atypical as it is a large pancreatic tumor with multiple metastatic lesions. With these limitations, it is estimated that 90% of insulinomas are benign, solitary tumors less than 2cm and up to 10% are malignant with metastasis to liver, lymph nodes, or bone. Prognosis is difficult to estimate and while there have been cases described of indolent metastatic disease and prolonged survival, most documented malignant insulinoma cases have poor prognosis with a median survival period of 2 years. There was no hepatomegaly, stigmata of chronic liver disease, murmurs or hypervolemia. Magnetic resonance imaging is typically reserved for long-term follow-up after an established diagnosis. Direct surgical visualization with histopathological confirmation is the diagnostic gold standard. Aggressive treatment with cytoreductive surgery and hyperthermic intraperitoneal chemotherapy prolongs life expectancy by several years, with a median survival of 53 months; this therapy is reserved for patients without extraperitoneal spread and adequate functional status. Systemic chemotherapy is an available alternative, but minimally improves survival. Due to the poor prognosis of this disease and the serious adverse therapy effects, early goals of care conversations are recommended. She was found to have intracellular parasites that were confirmed to be Babesia microti. Initial labs revealed parasite burden of 1% with acute anemia, evidence of hemolysis and abnormal liver function tests. The patient was transferred to the Intensive Care Unit where she received exchange transfusion without complication. Gaps in communication can contribute to delays in care, continuation of inadequate treatment and clinical errors. The Joint Commission has cited ineffective communication as a common root cause of sentinel events in hospitals. In case reports, some patients were treated with quinine and clindamycin as these agents are known to cross the placenta and there is more experience using quinine in pregnancy. Our patient progressed to severe disease despite being on antimicrobials given her risk factor of asplenia. Severe babesiosis may warrant exchange transfusion, but this had not been done in a pregnant patient before. To date, this is the first case of babesiosis in pregnancy requiring exchange transfusion. The driving factor influencing the outcome in this case was likely related to effective communication. Physician teams were able to collaborate on their expertise and evidence based knowledge to make a difficult clinical decision together. Two days prior to onset, she attended a party where she was in charge of making margaritas, a cocktail requiring lime and lemon juice. The following day, she went out boating on a sunny day in June, her symptoms developed upon waking up the next morning. Exam was notable for well-demarcated area of blanching erythema on the dorsum of hand as well as swelling of thumb, index and 4th finger. Small areas of hyperpigmented patches on right index finger and right ring fourth finger. In some cases where it presents as a hand print, it can be mistaken for child abuse. Careful history and examination can be used to differentiate phytophotodermatitis from other skin reactions. It usually presents as an irregular but well-demarcated lesion in handprint shapes or as drip marks. In severe cases, it can cause blistering as well as systemic symptoms related to toxicity such as fever, nausea, and vomiting. Avoidance of phototoxic agents and protection of skin from sunlight is recommended and can reduce further skin discoloration. Even though atrial myxomas are benign, risks of embolization are devastating, therefore, a high clinical suspicion with prompt diagnosis and early surgical resection is important. His rneurological deficits gradually improved and he was discharged 5 days post-surgery. Echocardiogram is the mainstay of diagnosis especially when there is concern for cardioembolic phenomena. Cardioembolic strokes account for 14-30% of ischemic strokes and atrial myxomas account for 0. Intravenous thrombolytic therapy with recombinant tissue plasminogen activator is recommended in acute ischemic stroke who present within the window period, but only a few cases of left atrial myxoma with ischemic stroke undergoing thrombolytic therapy have been reported. In a study of 6 of 10 patients who underwent thrombolysis, four improved symptomatically, one did not improve and one developed intracranial hemorrhage. Our patient had acute multifocal ischemic stroke, with a large atrial mass going through the mitral valve with each beat, presenting an enormous risk for embolism. Peripheral emboli to the limbs, eyes, and mesentery have been reported with delayed treatment, and no consensus has been made with regards to anticoagulation after hemorrhagic transformation. On Day 4 of admission, patient was febrile to 104F, hypotensive again to the 80s systolic, and hemoglobin dropped from 8. Initial infectious work-up returned positive for Clostridium perfringens on blood culture from two separate peripheral sites. Transthoracic Echo reported no signs of any vegetation, and Ultrasound of the abdomen demonstrated mild hepatomegaly with no signs of infection. After four days of vancomycin and meropenem treatment, he was transitioned to 14-day course of metronidazole (C. The disease often progresses rapidly to death, and therefore early recognition and immediate intervention are critical for patient survival.
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The patient had been evaluated at multiple clinics previously and discharged with reassurance cholesterol ratio too low order zocor 5 mg visa. Paracentesis yielded ascites that demonstrated a very elevated leukocyte count of 5 cholesterol ratio 5.1 purchase 10 mg zocor fast delivery,904 with 71% lymphocytes cholesterol test affected by food buy zocor 20 mg online, a protein of 5 cholesterol for hair buy 10 mg zocor with visa. A biopsy of the omentum demonstrated granulomas total cholesterol medical definition zocor 20mg, chronic inflammation cholesterol breakdown chart discount 10 mg zocor with amex, and rare acid-fast bacilli. It can also be caused by transmural translocation after ingestion of bacilli or through lymphatic channels from infected abdominal lymph nodes. Most commonly, patients present with ascites, abdominal pain, fever, and weight loss. Imaging commonly demonstrates ascites, peritoneal thickening, and lymphadenopathy. The gold standard of diagnosis remains laparoscopy with biopsy growing Mycobacterium on culture with caseating granulomas on histologic examination. Treatment has been controversial regarding suppressive therapy, but a randomized control trial proved that valacyclovir prophylaxis did not reduce recurrent meningitis compared to placebo. The prophylactic group had a higher risk of recurrence once valacyclovir was discontinued, likely from a rebound viral effect. Her first episode was bacterial, but all others were reported to be viral in nature. She was initially started on ceftriaxone, ciprofloxacin and acyclovir for empiric coverage. These antibiotics were de-escalated after 24 hours as she had rapid clinical improvement. Infectious diseases consultants recommended discontinuation of antibiotics or antivirals. Pain management complicated her hospitalization but she was discharged on hospital day 4. Milder forms of aseptic meningitis can mimic the life-threatening bacterial meningitis on clinical presentation. The disease is self-limited and patients will typically present with at least 3 or more episodes of fever and meningismus lasting 2-5 days. Physical exam was remarkable for diffuse abdominal tenderness with no palpable masses or organomegaly. Constitutional symptoms such as fevers, night sweats and chills are rarely present. Imaging studies are helpful for initial evaluation of pancreatic masses; however, a cytohistological analysis through biopsy is necessary for diagnosis and treatment. He had four out of five strength with dorsiflexion of both feet and an otherwise normal strength exam. He had absent lower extremity deep tendon reflexes bilaterally and hypoesthesia on the plantar region of his left foot. He underwent an L4 and L5 laminectomy with medial facetectomy for nerve root decompression. Postoperatively, he developed hypoesthesia of his feet, ankles, and hands as well as progressive ascending muscle weakness of his extremities followed by swallowing difficulty and shortness of breath. His progressive lower motor neuron deficits with new respiratory symptoms were consistent with a diagnosis of Guillain-Barre syndrome. The combination of autonomic dysfunction with lower extremity nerve pain, while not uncommon on presentation, differs from the classic symptomology of stocking hypoesthesia with progressive weakness. A methodical approach to determining the cause of the neuronal irritation is crucial in identifying the underlying cause of this problem. The most common etiology of lumbosacral radiculopathy is anatomical nerve root compression but nonanatomical causes must be considered. However noted associations commonly include viral illnesses, surgeries, and vaccines, most notably the flu vaccine. Pain due to nerve root irritation can be a presenting feature during the acute phase of Guillain-Barre in twothirds of patients. Seventy percent of patients have associated dysautonomia, with constipation/diarrhea being the most commonly reported. Decreased or absent reflexes are present in approximately ninety percent of patients at presentation. Significant complications can result from delayed diagnosis and treatment of Guillain-Barre, with up to 30% of patients requiring ventillatory support. It is essential that the general internist be able to differentiate this rapidly progressive cause of radicular back pain from the more common, less severe causes of back pain. Her past medical history was notable for a car accident 2 months prior resulting in clavicular, rib, L1 fracture status post percutaneous T11-L3 fixation. Physical exam revealed right eye chemosis, right proptosis, and bruit over right temple. The patient did not notice her right eye findings, until primary care provider astutely mentioned the subtle signs. Furthermore, it is an important reminder of potential late trauma associated complications. Patients usually present with ocular complaints related to increased ophthalmic venous congestion and ocular ischemia. Symptoms include pulsatile tinnitus, exophthalmia, chemosis, decreased visual acuity, headache, and diplopia. Interventional neuro-radiological approaches are the mainstays of treatment and are efficacious in 90% of cases. The main goals of treatment are symptom relief and preservation of arterial blood flow to the brain. It is important to counsel patients of potential complications of carotid sacrifice, emboli, and arterial dissection in Ehlers-Danlos patients. Her electrolytes, creatinine, white blood cell count, hemoglobin and platelet count were within normal limits. An abdominal ultrasound demonstrated a normal liver size, normal common bile duct, and an absent gallbladder. Potentially hepatotoxic medications were discontinued including isoniazid, quetiapine and chlorpromazine. Ischemic hepatitis, acute viral hepatitis, and drug-induced liver injury, often present with markedly elevated liver function tests - 25 times the upper limit of normal as in this case. When multiple potentially hepatotoxic etiologies are present and the cause of injury remains inconclusive, liver biopsy is indicated. Many medications have characteristic histological patterns of injury that can be revealed on biopsy. Of the remaining over 1000 drugs and herbal supplements documented to have caused liver injury, a significant portion, like isoniazid, are idiosyncratic-lacking an association between medication initiation or dose and onset of injury. Withdrawal of the offending agent remains the mainstay of therapy with the majority of patients experiencing complete recovery. The patient was started on ampicillin-sulbactam and surgery was consulted to investigate the lap band. The gastric band was subsequently deflated to relieve the obstruction and prevent re-aspiration. Imaging two weeks later revealed significant decrease in abscess size, decreased esophageal distention and improvement in respiratory symptoms. Findings of an abscess or empyema alter management in terms of antibiotics and pulmonary interventions if necessary. A thorough history is imperative due to risks associated with weight loss surgeries. Initial laboratory findings revealed an elevated total white blood cell count at 10. On day five of admission, a bronchoalveolar lavage of the right middle lobe revealed 16% eosinophils, which is highly elevated. The patient was placed on methylprednisolone and experienced significant improvement post-course. This chronically ill patient was being treated for a serious infection with broad, powerful antibiotics, but ended up requiring cessation of those antibiotics and steroids, despite not exactly falling within the criteria of a disease. The pathophysiology is thought to be immune-mediated resulting in the release of interleukin 5, which promotes eosinophil migration to the lungs. This may have interfered with the eosinophil yield as recent published case reports suggest the eosinophil percentage can be falsely low if the offending agent is stopped prior to testing. If alopecia is present, it is scarring, with raised hyperpigmented borders and central, depressed scar 1 and there is permanent loss of hair. More common causes of alopecia such as tinea capitis or alopecia areata are typically non-scarring. Determining risk factors for developing systemic lupus erythematosus in patients with discoid lupus erythematosus. However, a Computed Tomography of her brain at the time of trauma and repeated at the time of presentation did not reveal skull fracture. One month later, the mastoid lesions were unchanged, but similar lesions had appeared on her pinnae. She is currently being treated with clobetasone cream, with plans to start hydroxychloroquine. He began to feel "worn out" last week and has since had a mild productive cough and sinus congestion. He denies chest pain, dyspnea, palpitations, orthopnea, weight changes, or swelling. He maintains several social contacts and manages his own finances and medical care. Further evaluation is not indicated in the absence of symptoms or underlying disease. This case presents a unique clinical challenge due to a paucity of literature, as well as agerelated variables including functional status and increased therapeutic risk. Given his relatively good functional status, he may tolerate a beta blocker or even ablation if indicated, and gain quality-life-years. On the other hand, given his lack of symptoms and relatively increased risk of falls, procedural complications, or failure of therapy, a watchful approach may align better with his goals. Evaluation or intervention such as stress testing or catheterization would likely offer little benefit given his known high pretest probability and lack of symptoms. Furthermore, catheterization includes low but serious risk for adverse effects, which could worsen his function. Counseling should emphasize the importance of ongoing physical activity in prevention. He may tolerate other primary medical prevention, such as aspirin and statins, but the value of each should be discussed in the context of limited uncertain benefit and adverse effect assessment. If western blot does not confirm Lyme infection, or if an additional feature such as anemia is present, one should consider parvovirus as a source of infection. Parvovirus infection is diagnosed by testing for serum IgM, which is 89% sensitive and 99% specific in immunocompetent patients and remains detectable for two to three months after acute infection. She first experienced a headache and neck stiffness then developed myalgias and arthralgias that moved from her chest to her legs. She was treated with doxycycline for acute Lyme disease which was presumed to explain her symptoms but not her anemia. Further workup revealed co-infection with parvovirus, which can classically cause acute anemia. Parvovirus is often characterized by erythema infectiosum but can also present with similar symptomatic manifestations as Lyme disease such as arthralgias. Transient aplastic anemia is a complication of parvovirus that occurs more commonly in patients with decreased erythrocytes. Aplastic anemia is not associated with Lyme disease, so if present, this warrants further workup. The patient initially received 4 amps of bicarbonate and was subsequently placed on a bicarbonate drip. Likely attributing to this is the relatively safe pharmacologic profile of Metformin, availability, and cost. However, despite this, it is estimated that approximately 25% of patients taking metformin have one or more contraindications. Thus, the true indicidence is likely to be much higher than originally estimated in previous studies, and given the high mortality rate (30-50%), recognition and treatment of this potential complication are key. In patients with impaired renal function, metformin levels can achieve toxic levels quickly as it is renally excreted. Coupled with decreased conversion by the liver and kidney to glucose, lactic acidosis ensues. Patient was lost to follow-up but developed a severe polyneuropathy over several months which was thought to be a side effect of chemotherapy and started using a wheelchair. Physical exam showed distal glovestocking neuropathy, atrophy of the hands and feet with contractures, ataxia, and wide-based gait. Patient received carbamazepine for neuropathic pain and bendamustine and rituximab for advanced disease. Treatment is based on the extent of the proliferative disease, with radiation recommended for limited disease and chemotherapy for advanced disease with bone marrow involvement. Morbidity is largely based on the extent and spread of the peripheral sensorimotor neuropathy, which starts in the feet and spreads proximally.
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Since peripheral neuropathy can be caused by numerous factors, an investigation into the cause of the neuropathy should be undertaken as soon as the diagnosis of neuropathy is made. A characteristic pattern of numbness is one in which the distal portions of the nerves are first affected, the so-called "stocking-glove" pattern. This pattern occurs because nerve fibers are affected according to length of axon, without regard to root or nerve trunk distribution. Motor symptoms include weakness, which once again is distal, and typically involves extensor groups rather than flexor groups of muscles. Autonomic dysfunction is common and includes orthostasis, impotence in males and gastroparesis. A positive Romberg sign is frequently present due to proprioceptive loss in the lower extremities. Motor signs include distal weakness, primarily in extensor groups, and most prominent in the lower extremities initially. Distal muscles are often atrophic, and one should carefully assess the bulk of the extensor digitorum brevis muscles in the feet and of the intrinsic muscles of the hands. Muscle stretch reflexes are frequently lost, and most patients with peripheral neuropathy have absent ankle jerks as one of the first signs of the disorder. One helpful method is to consider four categories, namely etiology, distribution, pathology and modality. Etiology Most peripheral neuropathies fall into three etiologic categories, namely hereditary, toxic/metabolic, and those associated with systemic disease. Hereditary: this is a large group of disorders in which the onset of symptoms is insidious and progression is indolent over years or decades. This is the most common hereditary neuropathy that has an autosomal dominant pattern of inheritance. Phenotypic expression is often variable, such that affected family members of a propositus may have no symptoms and minimal neurologic findings. Characteristic clinical findings include striking atrophy of the calves, resulting in an inverted "champagne-bottle" appearance to the lower extremities. Large fiber sensory loss is present, with a marked reduction in vibratory perception and proprioception. Since this is a demyelinating polyneuropathy, nerve conduction velocity measurements are characteristically slow, at approximately 50% of normal values. This is a rare pediatric disorder with autosomal recessive inheritance that causes severe weakness and numbness, markedly enlarged peripheral nerves with "onion-bulb" formation and markedly slowed conduction velocities. This autosomal recessive disorder is caused by an enzymatic defect that results in accumulation of phytanic acid. The clinical triad includes peripheral neuropathy, retinitis pigmentosa and dry, scaly skin. Toxins: heavy metals including mercury, arsenic, lead, zinc and thallium; alcohol; and the organophosphates. A purely sensory neuropathy can be seen with several carcinomas, especially oat cell carcinoma of the lung. Diabetes mellitus is perhaps the most common cause of neuropathy in the United States. Mononeuropathy multiplex results in simultaneous dysfunction of several peripheral nerves, and is due to ischemic infarction of the vasa nervorum. Cranial neuropathies, truncal radiculopathies and diabetic amyotrophy (ischemic infarction of the lumbosacral plexus) are other forms of asymmetric neuropathies. Entrapment neuropathies, including carpal tunnel syndrome, are also commonly seen in diabetics. The reason for this is that the "offending agent" causing the neuropathy affects protein synthesis in the cell body of the peripheral nerve. Hence, neuronal dysfunction will first occur in the distal portions of the longest axons, and thus produce symptoms of weakness and numbness in the most distal portions of the extremities, i. Multifocal Neuropathies (Mononeuropathy Multiplex): Patients with these forms of neuropathy develop more-or-less simultaneous dysfunction of several peripheral nerves. Prognosis for recovery is good, assuming that the underlying disease process leading to nerve infarction can be suppressed. Distal Axonopathy: In this form of neuropathy, a metabolic abnormality causes failure of protein synthesis and axonal transport, resulting in degeneration of distal regions of axons. For this reason, axonal neuropathies characteristically produce a "stocking-glove" distribution of numbness and weakness. Small-diameter axons are most susceptible to metabolic injury because of their small neuronal size and lack of "reserve". Hence, initial symptoms of an axonal neuropathy typically include autonomic dysfunction and small-fiber sensory modalities, including loss of pain and temperature perception, since these modalities are subserved by small, unmyelinated or thinly myelinated axons. Myelinopathy: An immune-mediated attack on peripheral nervous system myelin is the characteristic pathologic change in this group of neuropathies. In both of these neuropathies antibodies have been found that cross-react with peripheral nerve myelin. In general, demyelinating neuropathies affect large-diameter, myelinated axons at the start of the illness, and hence produce significant motor weakness and large-fiber sensory loss, including loss of vibratory perception and proprioception. Neuronopathy: Selective involvement of the cell bodies of motor, sensory and autonomic nerves is the hallmark of this group of neuropathies. Amyotrophic lateral sclerosis and the spinal muscular atrophies are two examples of somatic motor neuronopathies. Somatic sensory neuronopathies result from disruption of the metabolism of sensory nerve cell bodies, followed by degeneration of their processes. Special permeability of the blood vessels in the dorsal root and Gasserian ganglia make these neurons particularly vulnerable to certain toxins. Autonomic Neuronopathy: this unusual group of neuropathies results from isolated involvement of post-ganglionic autonomic neurons and causes idiopathic orthostatic hypotension. The pathologic lesion in this group of neuropathies is confined to the cell bodies. Mixed-Modality Neuropathies: the majority of peripheral neuropathies is not modality-specific, and includes various combinations of motor, sensory and autonomic dysfunction. The reason for this finding is that most peripheral nerves include a mixture of motor, sensory and autonomic axons. Likewise, since most axons are myelinated to a greater or lesser extent, demyelinating neuropathies also produce a mixture of motor, sensory and autonomic symptoms. Electrodiagnostic studies are helpful in quantitating the neuropathy, while blood and urine studies are helpful in identifying an etiology. Electrodiagnostic Studies Nerve Conduction Study: the recording and measurement of the compound nerve and muscle action potential elicited in response to a single supramaximal electrical stimulus, to measure the terminal latency, amplitude and duration of the evoked potential, as well as the conduction velocity. Nerve conduction studies are helpful in documenting that a neuropathy exists, quantitating the severity, and noting the distribution of the neuropathy, i. In addition, nerve conduction studies can provide information on the modality involved, i. Demyelinating neuropathies (neuropathies due to loss or destruction of myelin) result in slowed conduction velocities and prolonged distal latencies, because conduction velocity is proportional to the velocity of the largest-diameter myelinated fibers. Axonal neuropathies (neuropathies due to loss of axons or their cell bodies) generally result in a reduced amplitude of the compound motor or sensory nerve action potentials. This test allows one to physiologically evaluate the motor unit, including the anterior horn cell, peripheral nerve, and muscle. Chronic Denervation: Voluntary motor unit potentials are of large amplitude and long duration, and are frequently polyphasic, because the motor units are enlarged as a result of re-innervation of adjacent previously denervated muscle fibers. Recruitment of additional motor units in response to increasing the force of muscular contraction is reduced for the same reason. Demyelinating Neuropathy: A decreased recruitment pattern is seen, since demyelination interferes with conduction of individual action potentials along the course of a peripheral nerve. Because denervation and reinnervation of muscle fibers are not features of demyelinating neuropathies, the configuration of the voluntary motor unit potentials is usually normal, and fibrillation potentials are not seen. In general, a nerve biopsy is performed to evaluate asymmetric, multi-focal neuropathies. The sural nerve is frequently biopsied, since this is a purely sensory nerve that is easily obtained. In the upper extremity, the superficial radial nerve may be biopsied if necessary. The nerve specimen is typically evaluated by means of light and electron microscopy. Semi-thin plastic embedded sections, stained with toluidine blue, are helpful for evaluating the myelin sheaths. Teased nerve fiber preparations are also helpful to look for demyelination and remyelination. Vasculitis, amyloidosis, leprosy and sarcoidosis can be accurately diagnosed by means of nerve biopsy. Performing a nerve biopsy routinely in the evaluation of symmetric, distal polyneuropathies is usually fruitless, in that the pathologic diagnosis most often reveals "chronic neuropathy with mixed axonal-demyelinating features", a non-specific finding of little clinical benefit. Blood Studies Routine blood studies should be obtained in all patients with peripheral neuropathy in order to screen for reversible causes. Since nerves regenerate slowly, at a rate of about one mm per day, recovery is often prolonged and may take months to years. Corticosteroids may be given daily or on an every-other-day regimen, depending on the severity and tempo of the disease. The typical initial dose of corticosteroids for the treatment of these neuropathies is 1 mg/kg/day of prednisone (or 2 mg/kg every-other-day). Corticosteroids have never been proven to be effective in treating Guillain-Barre syndrome, and hence are not recommended for this disorder. Immunosuppressives: Azathioprine, cyclophosphamide, cyclosporine, mycophenolate and methotrexate are all used in the treatment of autoimmune diseases. Azathioprine is frequently used, in combination with steroids, to treat autoimmune neuropathies because of its steroid-sparing effect. Concurrent use of these two medications allows corticosteroids to be tapered more quickly and more completely once the neuropathy is brought under control. This medication has a delayed beneficial effect and several months are required before an effect may be seen. Azathioprine is metabolized by xanthine oxidase, and medications that block this enzyme, such as allopurinol, should be avoided since concurrent use can cause azathioprine toxicity. Plasmapheresis: In this procedure, blood is removed from the patient, plasma is separated from blood cells and discarded, and blood cells are resuspended in colloid solution and reinfused. The effects of plasma exchange can be summarized as "fast, temporary, and expensive". Symptomatic Treatment Numerous symptomatic treatments for the pain of peripheral neuropathy are available, and all have their relative risks and benefits. Tricyclic Compounds: Drugs in this category include amitriptyline, nortriptyline, desiprimine, imiprimine and duloxetine. These drugs inhibit the re-uptake of the catecholamine neurotransmitters epinephrine and norepinephrine as well as serotonin, and thus may enhance central pathways that suppress pain transmission. The tricyclic compounds are quite useful for treatment of the burning, dysesthetic pains seen with peripheral neuropathies. Effective dosages of these drugs for treating chronic neuropathic pain are typically lower than the dosages used for treating depression. We recommend starting with a low single dose at bedtime and slowly increasing the dose over several weeks. Patients should be informed that it may take several weeks before full therapeutic effects are realized. These drugs stabilize neuronal membranes and may thus prevent neuronal "shortcircuits" that lead to neuropathic pain. The anticonvulsant drugs are quite useful in treating the lancinating pains frequently seen with trigeminal neuralgia and in some other peripheral neuropathies. Effective dosages for treating neuropathic pain are similar to the dosages used for treating seizures. Lamotrigine, a new anti-seizure drug effective for primary generalized seizures, can cause a severe and fatal cutaneous hypersensitivity reaction if the starting dosage is high, and therefore must be started at a very low dose with a very gradual dosage escalation. Topicals: Capsaicin, a drug that impedes pain transmission by depleting substance P from sensory nerve fibers, has been found effective in treating refractory neuralgia in several studies. The cream must be applied several times daily to be effective, and patients frequently experience severe burning following each application for one or two weeks following initiation of treatment. Transdermal lidocaine (Lidoderm), a local anesthetic, also appears to be effective for some patients with neuropathic pain syndromes.
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