Лактирующая аденома молочной железы у беременной женщины – клинический случай

Idiopathic granulomatous mastitis (IGM) is a rare inflammatory breast disease mimicking carcinoma and puerperal or non-puerperal mastitis. The primary purpose of this prospectively performed case control study was to compare clinical and imaging signs of IGM with the reference group of nonspecific, non- puerperal mastitis (NM) to identify the most typical clinical and imaging signs essential for a correct differential diagnosis. The secondary purpose was to present a new approach to non-invasive treatment. Thirty-nine women with histologically proven IGM and twenty-six patients with nonspecific mastitis underwent clinical examination, breast ultrasound (US), mammography (MG) and MRI examination. The most typical signs were selected for each group, and method and were statistically evaluated. The effectivity of colchicine, vitamin E and ribwort plantain tincture in treatment was assessed by clinical examination and imaging. Typical clinical signs of IGM included unilateral acute onset of breast edema, redness, palpable masses, missing fever, lymphadenopathy, no response to antibiotics or surgical interventions. Ultrasound revealed: "finger-like" structures (100%), ductectasias (76.9%), abscesses (76.9%), and lymphadenopathy (15.4%), while in MRI skin and tissue edema (100%), multicentric lesions (100%), abscesses (76.9%), ring enhancement (84.6%), lymphadenopathy (15.4%) and small enhancing lymph nodes (38.5%) were observed. Among the clinical signs, fistulas, hypoechoic mass, ductectasias and diffusion weighted images (DWI) restriction were significantly more frequent in patients with IGM than in those with NM. Treatment effectivity yielded 100% with a complete response between 6-19 months, depending on the disease extent. Targeted questions together with imaging can speed up selection for proper treatment with colchicine, vitamin E and local treatment. Long lasting use of antibiotics and repeated surgical interventions should be avoided.

Cushing's syndrome (CS) during pregnancy is a rare endocrine disorder characterized by hypercortisolism, which is significantly associated with maternal-fetal complications. Despite its rarity, CS during pregnancy may be related to a high risk of complications for both the mother and fetus.The aim of the present case study is to update the diagnostic approach to CS during pregnancy and the therapeutic strategies for this medical condition to minimize maternal-fetal complications. Here, we present two cases of CS in pregnant women, one of whom had twins. Typical clinical symptoms and signs of hypercortisolism developed at the beginning of pregnancy. The plasma cortisol diurnal rhythm of the pregnant patient was absent. CS was confirmed by cortisol and adrenocorticotropic hormone (ACTH) assessment, as well as imaging examination. We investigated the changes in the hypothalamic-pituitary-adrenal axis during normal pregnancy and the etiology, diagnosis and treatment of CS during pregnancy. Due to the associated risks of laparoscopic adrenalectomy,it is uncertain whether this treatment significantly decreases overall maternal mortality. Additional observational research and validation through randomized controlled trials (RCTs) are required. We advise that CS in pregnant women be diagnosed and treated by experienced teams in relevant departments and medical centers.

ACUTE compartment syndrome (ACS) represents a limb-threatening condition. Delaying diagnosis and therapy may lead to irreversible neuromuscular ischemic damages with subsequent functional deficits.1 Diagnosis is primarily clinical and characterized by a pain level that quality exceeds the clinical situation. Diagnosis is assessed by invasive pressure monitoring within the suspected compartment. Once ACS has been confirmed it represents a surgical emergency with definitive treatment requiring immediate fasciotomy to relieve the pressure within the affected compartment. Irreversible tissue damage can occur within 4–6 h after the onset of symptoms. However, nerves are already seriously damaged after 2 h of increased compartment pressure.1,2 Concerns about masking pain as cardinal symptom and therefore leading to a delay in diagnosis and therapy have been raised in connection with regional anesthesia.3,4 Moreover, several case reports and case series have blamed different types of regional anesthesia4–11 and even the use of opioid patient-controlled analgesia12 for delaying diagnosis of ACS. Therefore, the use of regional anesthesia for trauma and orthopedic surgery remains controversial.4,6,13 A case involving continuous regional anesthesia of the upper extremity and the development of an ACS is presented.A 47-yr-old woman was scheduled for surgical treatment of a complex distal humerus fracture of her right dominant arm. Medical history was unremarkable except for obesity (body mass index 41.5), a metabolic syndrome (diabetes, obesity, and hyperlipidemia), and sulfazine treatment due to Crohn disease. The right arm showed classical signs of hematoma and swelling without any clinical sign for increased compartment pressure. All nerve functions were preserved. An open reposition of the fracture, osteosynthesis of the capitulum, trochlea humeri, and radial condylus were performed with postoperative placement of an open arm splint. The anesthetic management combined infraclavicular catheter, placed preoperatively but no local anesthetic was given until after the patient has been extubated, and general anesthesia performed with target-controlled infusion of propofol (Disoprivan®, AstraZeneca, Zug, Switzerland) and remifentanil (Ultiva®, GlaxoSmithKline, Münchenbuchsee, Switzerland). Infraclavicular catheter placement and general anesthesia were uneventful including stable patient’s hemodynamic parameters during the 150 min lasting surgical intervention. After extubation, the sensomotor function of the operated arm was checked by the surgeons and the infraclavicular catheter was started thereafter. An initial bolus of 30 ml ropivacaine 0.5% (Naropin®, AstraZeneca) was applied with intermittent aspiration, and block assessment indicated a successful block. The patient was transferred to the postoperative care unit for further observation and a patient-controlled regional analgesia infusion with ropivacaine 0.3% (Naropin®) was started with a continuous rate of 6 ml/h, an additional bolus of 5 ml with a lockout time of 20 min. Additionally, acetaminophen (Perfalgan®, Bristol-Myers Squibb, Baar, Switzerland) 4 × 1 g/day was prescribed.During the first 2 h in the postoperative care unit, the patient did not complain about pain, hemodynamic parameters remained within normal range, and peripheral pulses were present. The wound drainage showed 70 ml blood loss before discharge to ward and assessment of the infraclavicular catheter revealed a good function.Patient’s pain assessed on the visual analog scale was 10/100 during the first postoperative night without the need for additional analgesics. Fourteen hours after surgery she developed severe forearm pain (visual analog scale 90/100). The anesthesia resident on call found a sensory and motor block of all target territories/muscles in the hand but a preserved contraction of the biceps and coracobrachial muscles. Suspecting a not blocked musculocutaneous nerve being responsible for the increasing pain she administered an additional bolus of 20 ml ropivacaine 0.5%. The severe pain was still present 20 min after its administration despite the occurrence of a new complete motor and sensory block of all territories. The characteristics of the breakthrough pain alarmed the anesthesiologist who suspected an incipient ACS. The orthopedic surgeons were informed and observed an intense pain on the dorsolateral part of the right forearm in the area of the extensor compartment with a significant increase in pain with stretching of these muscles. The intracompartmental pressure was measured using the Stryker Intra-Compartmental Pressure Monitor System (Stryker®, Kalamazoo, MI). The pressure in this compartment was 40 mmHg. Emergency fasciotomy of the extensor compartment of the forearm was performed under general anesthesia within 1 h after assessment of intracompartmental pressure. Intraoperatively, the extensor compartment of the forearm was greatly swollen and very tense. Upon decompression, the muscles were edematous but viable. Further exploration of the wound revealed two hematomas which were evacuated but no other compartments (of the forearm or arm) were under tension. The fascia of the extensor compartment was left open but the skin could be closed without any problem. Therefore, primary wound closure was performed. The infraclavicular catheter was removed. The motor and sensory function returned to normal after 4 h. The patient made an uneventful recovery and was discharged 3 days later. The follow up at 3 months showed no sensory or motor disabilities of the operated arm.ACS is defined as an increase of pressure within a fixed osteofascial anatomic space, leading due to decreased local tissue perfusion to an impairment of cellular function and, when sustained, to irreversible changes like infarction of muscles and nerves in the compartment. Important variables affecting the outcome are the amount and the duration of pressurization and the extent and severity of soft tissue injury.14The different symptoms and signs describing ACS are reported in table 1. Although previous studies have reported that resting interstitial tissue pressures in the healthy vary between 0 and 8 mmHg for the dorsal and volar forearm compartments and less than 15 mmHg in the interosseous muscles of the hand15 pressure measurement is considered to be accurate. Interstitial tissue pressure measurement is measure point dependent in noninjured15 and injured extremities with higher pressures within 5 cm of the fracture.16Different absolute compartment pressures or calculated pressures (difference between systolic or mean arterial pressure and the compartment pressure) have been described in the literature.17,18 Although the mean arterial pressure for the difference calculation (mean arterial pressure—compartmental pressure) seems to be more accurate comparative, clinical trials are lacking. It must be emphasized that much of above work exclude children and was mainly carried out studying ACS of the lower extremity. Upper extremities might have other pressure thresholds but due to lacking evidence the established threshold of ΔP 30mmHg is retained. In children, the mean arterial pressure rather than the diastolic pressure has been suggested to calculate the ΔP as the diastolic blood pressure is often lower in children.19Data from the Royal Infirmary of Edinburgh show an average annual incidence of 3.1 per 100,000 people (7.3 per 100,000 men and 0.7 per 100,000 women).17The key element is the elevation of tissue pressure within encapsulated muscles. In the ACS, fluid shifts between the blood and the extra- and intracellular space due to an increased tissue pressure of the compartment leading to an increased extravascular venous pressure. Further pressure leads to a decrease of capillary blood flow and decrease in tissue Po2 ending in a metabolic deficit. The end stage is deficit muscle ischemia and necrosis. Tissue metabolism requires an oxygen tension of 5–7 mmHg. This tension is maintained by capillary perfusion pressure of 25 mmHg which is above the normal interstitial tissue pressure of 4–6 mmHg. The tissue perfusion pressure equals capillary perfusion pressure minus interstitial pressure. When tissue pressures reach 30–40 mmHg,20 the extraluminal pressure causes progressive arteriole collapse due to direct pressure effects and to interferences with critical closing pressures leading to local tissue hypoxia with secondary shunting to areas with less vascular resistance. Moreover, local tissue perfusion ceases when the interstitial tissue pressure equals the diastolic blood pressure. The rising tissue pressure causes collapse of the veins. Arterial flow increases the venous pressure reestablishing the flow, but the increased venous pressure adversely affects the arteriovenous gradient with consecutive ischemia21 (fig. 1).Two pathophysiology theories are the “arteriovenous gradient theory” and the “ischemia–reperfusion syndrome.”22 Both theories share the increasing tissue pressure, the consequently decreasing capillary blood flow, and the decrease of tissue Po2 resulting in a metabolic deficit. If the ACS is caused either by external pressure or by an increased internal pressure, first the arteriovenous gradient theory explains the reduced capillary blood flow with increasing venous pressure or increasing capillary resistance. In the case of additional injuries leading to hypovolemic shock, the “arteriovenous gradient theory” explains the diminished arterial pressure resulting in reduced capillary blood flow. In the case of reperfusion after revascularization or tourniquet release, the “ischemia–reperfusion mechanism” explains how different factors such as the release of oxygen-free radicals, massive accumulation of calcium in the ischemic muscles, and the infiltration of neutrophils into the reperfused vessels lead to an increase in compartment pressure. The hypoxic injury releases vasoactive substances, which increase the endothelial permeability. Subsequently, this mechanism leads capillary leakage into the extravascular space provoking additional edema and additional rise in compartment pressure. The falling pH and the degradation products contribute to a further increase in the tissue pressure, thereby reducing microperfusion as explained by the “arteriovenous gradient theory” leading to a self-perpetuating vicious circle. As a result of ischemia nerve conduction slows down.However, several authors have demonstrated that early decompression leads to a drop in extraluminal pressure, restoration of local blood flow, removal of anaerobic metabolites, and return of normal cellular function.23 Cells may become edematous and demonstrate histological evidence of injury after decompression, but the morphology and function of most of them will return to normal within some days.Pain is considered to be the main clinical symptom of a developing ACS. Pain exceeding clinical expectance, pain not responding to analgesics, palpable tenseness in the affected compartment and pain worsening with passive stretching of the muscles in the according compartment are the most accurate early indicators. Paresthesia, paresis, and pulselessness are in most circumstances late signs of an ACS and already indicating a potentially irreversible compartment and muscle damage. However, pain may not be useful in children or in adults with an altered level of consciousness.1Commonly used signs in clinical practice are neither reliable nor sufficiently specific or sensitive if there are not at least three signs.24 Pulselessness in fact is considered to be a late sign and is associated with bad prognosis.4,18 Even pain is unreliable if there is no breakthrough pain or increasing analgesic demand.4 In fact, the simple presence of pain was insufficient to prevent from delaying ACS diagnosis.25–27 Even the clinical palpation of the tense and swollen extremity has been shown to be strongly assessor dependent and unreliable with a sensitivity of 24% and specificity of 55%.28 Paresthesia and other altered sensations are also of questionable diagnostic value due to many confounders like central acting analgesics, alcohol, brain and spine injuries, altered level of sensation, other distracting injuries, extremes of age, language, and ethnical barriers.1 Despite these limitations arguments against regional anesthesia or even opioid patient-controlled analgesia focus on the possible interference of these techniques with the classical signs of ACS.2,3The reference method for diagnosis of ACS remains the measurement of interstitial tissue pressures. Different methods for measuring intracompartmental pressure have been described to directly, indirectly, or continuously measure compartment pressure29 (table 2). There are less invasive new technologies like laser doppler flowmetry and 99Tcm-methoxy-isobutryl isonitril scintigraphy. However, it is unclear how practical and cost-effective these methods are in clinical practice. An interesting development in the field of noninvasive measurement techniques was introduced by the near-infrared spectroscopy which detects changes and trends in relative oxygen saturation of hemoglobin. In the setting of ongoing ACS, near-infrared spectroscopy has been described to have a high sensitivity and specificity detecting and providing continuous monitoring of intracompartmental ischemia and hypoxia.30 However, more studies are warranted to define the correlation with critical pressure thresholds. Magnetic resonance imaging and scintigraphy are not sensitive enough to be recommended for ACS diagnosis.In the case of an incipient compartment syndrome, frequent clinical reevaluation must be completed and accurately documented.14 Casts and circumferential dressings must be removed and positioning with tension or distorsion must be avoided to not further compromise blood flow. Fluid therapy must be carefully evaluated, electrolytes, renal function, coagulation, and hemodynamic parameters must be monitored. Once the diagnosis of ACS has been established, surgical decompression of the affected osseofascial compartments is warranted.31The most outcome relevant factors are fasciotomy, timing of diagnosis and fasciotomy performance, and the concomitant injuries. However, for the ACS of the upper extremities controversial opinions exist. Good results are reported after early diagnosis and quick fasciotomy, poor results with delayed treatment. However, there is no prospective study documenting the benefit of early fasciotomy for upper extremity ACS.32Delaying fasciotomy for more than 12 h has been shown to significantly worsen outcome.16 According to Hayakawa et al.33 fasctiotomy performed by 6 h after diagnosis of ACS led to a satisfactory outcome in 88% of cases with an amputation rate of 3.2% and 2% deaths, whereas fasciotomy after 12 h showed satisfactory outcome in only 15% of cases with 14% amputations and 4.3% deaths. There is sparse data about the timeframe >6 h but <12 h, as residual deficits happen also if fasciotomy is performed only 2 h after ACS diagnosis.34Regional anesthesia in patients at risk for developing an ACS is a highly controversial topic discussed.2,3,35 However, there is no randomized trial comparing outcome after different anesthesia managements. Actual clinical practice is based only on case reports, retrospective case series, recommendations and reviews, and the belief that regional anesthesia completely blocks pain and alters sensory-motor response to impede diagnosis of ACS.4 Advances in regional anesthesia techniques, drugs, and concentrations which allow a goal-directed therapy of pain with spare of sensory-motor functions are ignored.This patient presents an ACS of the upper extremity involving regional anesthesia. Interestingly, some of the published case reports blame a peripheral nerve block (PNB) for masking an ACS in a territory not covered by the block. This challenges the sole responsibility of the PNB in masking the ACS.7,10 There is one recent case report blaming continuous perineural blocks for delaying diagnosis of ACS after distal femur and proximal tibia osteotomy.5 Additional to general anesthesia continuous sciatic and femoral nerve blocks were run with ropivacaine 0.2% after an initial bolus of 30 ml ropivacaine 0.5% through each catheter. Due to persistent breakthrough pain on postoperative day 2 the surgeon performed a clinical evaluation (dense swollen gastrocnemius muscle, excruciating upon passive plantar flexion, and dorsiflexion of the foot) and a compartment pressure measurement (30 mmHg). Despite these findings, a reevaluation was performed 2 h later showing the same findings. Finally, an emergent decompressive fasciotomy was performed. Once again, the breakthrough pain was ignored. This delay had serious consequences: tissue loss and functional deficits resulted. A second case report using continuous popliteal nerve block describes a patient who was sent home on postoperative day 1 with a popliteal catheter after foot surgery despite a dense motor and sensory block.11 Pain became worse overnight and presented to the emergency department on postoperative day 2. The cast was splinted but not removed, no compartment pressures were measured. Patient refused to have the continuous PNB removed and was managed through the telephone. On postoperative day 4 the catheter was removed uneventfully. Probably, this is not a case of ACS but of pressure pain induced by tight cast which could have led to an ACS. However, patient management in this case report is not according to common standard. The case described by Noorpuri et al.9 describes an ACS after an ankle block for a revisional forefoot arthroplasty. The patient developed increasing pain despite receiving supplementary analgesia, paresthesia, motor weakness and showed a tense swollen forefoot with a delayed capillary refill. No compartment pressure monitoring was performed and fasciotomy was performed due to increment clinical signs. Despite the neglect of typical clinical signs the authors blamed the ankle block for masking the ACS and delaying its diagnosis.None of the five currently published case reports blaming peripheral regional analgesia for delaying diagnosis or therapy of ACS can stand a thorough study of the case. Ignored increasing pain and typical clinical signs are present in all cases and in one regional anesthesia did not even block the area of interest.Our case shows the development of an ACS in a patient treated for analgesia using an infraclavicular catheter. As reported in section IV and in table 3 we suggest not to activate the perineural catheters in patients the surgeons consider to be at risk for either surgery associated nerve damage or compartment syndrome. This allows an immediate testing after surgery without delay in diagnosis. In the case of high risk for an ACS a delay in starting the catheter can be wise or the application of a very low concentration of local anesthetics preventing motor block might be suggested.In this case the ACS developed slowly and breakthrough pain was a symptom. The resident evaluated the pain as postsurgical due to the motor function of the biceps and coracobrachial muscles. The fingers were according to her first description not swollen. Interesting is the fact that despite 20 ml 0.5% ropivacaine after 20 min the pain was still present despite the occurrence of a new complete motor block. This and the measured compartment pressure were the only clinical signs. The swelling was only appreciated after removal of the splint. This further suggests, that at least for PNB, regional anesthesia does not mask the cardinal symptom of ACS: breakthrough pain. However, the typically used 0.5% concentration for the top up of the catheters should be reconsidered in patients at risk for ACS. What would happen with our patient if pain had improved by 50%? Moreover, the communication between anesthesiologist and surgeons remains to be of pivotal importance. ACS is a surgical diagnosis and therefore patients with unclear pain must be evaluated by both, anesthesiologist and surgeon.There is no single case report showing a delay in ACS diagnosis due to peripheral regional anesthesia, even considering continuous regional anesthesia. Almost all published cases including epidural analgesia (EDA) showed that patient complained of increasing pain despite regional anesthesia,10 loss of motor function despite reduction of local anesthetic concentration36 or increasing analgesic demand.4,5,11 Only in two cases was a dense motor block noted after EDA at time point of ACS diagnosis.26,37 Other cases even blamed a continuous PNB for an ACS in a territory the block did not cover.7,10 The other case reports did not give any details about documentation or patient management before start of symptoms/clinical signs.4 Therefore, regional anesthesia can only be considered to be associated but not the cause of the delay in diagnosis. Excluding both cases with dense motor block after EDA26,37 there was no evidence that regional anesthesia masked important symptoms of compartment syndrome.Despite this evidence, the use of regional anesthesia for patients at risk for ACS remains a topic of dispute between anesthetists and surgeons.3 As reported by Cascio et al.38 a good, standardized documentation improved the awareness of this complex diagnosis. However, in a retrospective study of preoperative medical records of 30 consecutive patients who underwent for ACS, documentation was in patient a high level of with postoperative clinical and if invasive monitoring are of must be at least in a in the case of new or findings, the of assessment must be The classical are of unreliable in the presence of regional anesthesia and should therefore be by the clinical signs and of As described by et increasing analgesia changes by an average of h However, in cases of compartment syndrome the average time to surgical decompression from the increase in analgesia was which were in our with the orthopedic surgeons are presented in table The of regional anesthesia is if there are general anesthesia or central blocks like anesthesia, to surgery time should be The of anesthesia in the of testing motor and sensory function after surgery and therefore to a for further clinical at high risk for general anesthesia and with a surgery time the duration time of and local anesthetics can benefit from a continuous anesthesia which as the of the local anesthetic can be to the surgery as to application should not be used for analgesia the level of the surgical block is more to If general anesthesia is a of EDA with anesthesia considering the described above are EDA should not be started until the surgeon has made the clinical low concentration of ropivacaine can be as the on motor function is must be considered from case to case. with or without is possible but not considered as a first As EDA is the most blamed in for delaying diagnosis of ACS its use should be and should be However, with EDA dense motor blocks must be avoided and if techniques are PNB are only recommended if postoperative pain is not a with low on motor function after surgery are are the to our In cases of high risk for an ACS, general anesthesia is combined with a continuous PNB which is placed but not started continuous before general anesthesia until postoperative evaluation is performed. Pain therapy is performed with low of in with remifentanil target infusion or even remifentanil until start of continuous This allows a timing with the surgeon but requires that catheters are placed without first local anesthetic through the The catheter should be started with a low concentration bolus of ml ropivacaine to initial motor function loss and with a continuous infusion patient-controlled using ropivacaine 0.2% ml/h, bolus out 0.3% has been shown not to motor to 0.2% for block and could be used in an for surgery under continuous However, according to our using a bolus of ropivacaine might lead to a motor block and should for be avoided in this wound infusion or are not even using ropivacaine pathophysiology of ischemic pain is highly complex and is by and acting on ischemia it is that and are some of the leading to ischemic pain. Tissue the pain acting on muscle resulting in pain and leading to a of with et who that compartment ischemia can lead to an regional anesthesia with 0.2% In our ropivacaine 0.3% was and breakthrough pain was still present even after a bolus with 0.5% It would be interesting to the concentration and for bolus application and continuous infusion to use regional anesthesia as an and early of increased muscle anesthetics on the The is the main for pain in the peripheral of this for the postoperative could be of for patients at risk for ACS and for continuous PNB motor outcome studies with the and of intracompartmental pressure monitoring and data on the diagnostic characteristics of intracompartmental pressure monitoring are Moreover, the critical ΔP for other of the and for children must be

The impact of chicken infectious anemia virus (CIAV) infection on commercial chicken flocks in Israel was examined by analyzing flocks with or without typical CIAV signs, signs of other diseases, or apparently healthy flocks. In 23 flocks (broilers and layers) of ages up to 8 wk, typical signs of CIAV infection (stunting, gangrenous dermatitis, and secondary bacterial infections) were recorded. When permitted by flock owners, in several cases among these 23 flocks the morbidity, mortality, and performance parameters were recorded; the presence of CIAV was detected by polymerase chain reaction (PCR); and the antibody status of parents and broilers was measured. In addition, total mortality, number of birds sold, total kilograms of meat sold, density (kg/m2), mean age at slaughter, daily growth rate in grams, total kilogram of food consumed, food conversion rate, and the European Index were calculated. We also surveyed flocks affected by other diseases, such as tumors, respiratory diseases, or coccidiosis, and flocks with no apparent clinical signs. The latter flocks were negative by CIAV-PCR, indicating that typical CIAV clinical signs are associated with one-step PCR-CIAV amplification. However, a small amount of CIAV might still be present in these flocks, acting to induce the subclinical effects of CIAV infection. These data indicate a link between the presence of virus sequences and typical CIAV signs and strengthen the concept that CIAV infection has a negative economic impact on the chicken industry.

To compare clinical characteristics and laboratory findings of dogs with eclampsia with those of dogs without eclampsia. Retrospective study. 31 dogs with eclampsia (affected) and 31 with dystocia (controls). Information on signalment, type of diet, reproductive history, litter size, time from whelping to eclampsia, body weight, clinical signs, results of physical examination and hematologic and biochemical analyses, response to calcium supplementation, and recurrence was obtained from the medical records of all dogs with eclampsia evaluated between 1995 and 1998 and compared with information from medical records of 31 of 102 dogs with dystocia evaluated during the same period. Dogs with eclampsia weighed less, had a smaller body weight-to-litter size ratio, higher rectal temperature and heart and respiratory rates, and lower plasma total solids concentration than control dogs. Ionized calcium concentration was < or = 0.8 mmol/L for all but 1 of the affected dogs; median concentration for the affected dogs was significantly less than that for control dogs. Six (19%) dogs did not manifest typical clinical signs associated with eclampsia. Twelve (39%) dogs with eclampsia had previous litters; none had a history of eclampsia. Affected dogs were discharged from the hospital within hours after admission, but 3 dogs returned 1 to 3 weeks later because of recurrence of eclampsia. Eclampsia develops primarily in small-breed dogs with large litters. Plasma ionized calcium concentrations > 0.8 mmol/L in dogs with clinical signs typical of hypocalcemia may indicate that other causes of clinical signs should be considered. In addition, some dogs with eclampsia may have low ionized calcium concentrations and not manifest typical clinical signs.

Immunohistochemistry in the classification of systemic forms of amyloidosis: a systematic investigation of 117 patients

Background: Infectious diseases have expanded their host and geographic ranges, increasing impacts on both human and animal health. Mycoplasma gallisepticum usually causes avian chronic respiratory conditions and Histomonas meleagridis infects the cecum and the liver of poultry. Although these diseases have been reported in several bird species, information associated with their prevalence and impact in local flocks of ornamental birds is scarce. This communication describes severe outbreaks of mycoplasmosis and histomoniasis that affected a southern Brazilian commercial flock of ornamental birds.Case: The outbreaks occurred in an ornamental bird flock that contained 2,340 birds from 39 different species, distributed mostly in the orders Galliformes, Anseriformes, and Psittaciformes. Mycoplasma gallisepticum affected 12 chukar partridges, 12 Indian peacocks, 19 ornamental chickens and 46 individuals of 4 species of pheasant. The disease cases were distributed between April and July 2015. A total of 36 birds died due to the disease’ complications and most surviving birds suffered from severe ocular sequels, which determined their subsequent culling, despite attempts of different treatment protocols. The main signs included coughing, sneezing, infraorbital swelling, wasting, and death which were mostly associated with caseous sinusitis. Affected birds had positive samples when stained with anti-Mycoplasma gallisepticum immunohistochemistry and tested by Mycoplasma gallisepticum-Polymerase Chain Reaction. The application of 2 doses of a Mycoplasma gallisepticum vaccine in early 2016 to all the Galliformes in the flock reduced the annual prevalence to 4 clinical cases. Histomoniasis affected and killed 19 out of 27 chukar partridges that were being kept with ring-necked pheasants in the same enclosure. The disease occurred between September and December 2016 and a high prevalence of Heterakis gallinarum was detected in the flock. The main findings included apathy and death linked to hepatic and cecal necrosis. Admixed in the necrotic areas, there were numerous round to oval, eosinophilic, protozoal trophozoites of 15-20 µm in diameter, occasionally containing a 3-5 µm centrally located basophilic nucleus (histomonads) surrounded by a clear halo. Anthelmintic dosing, exchanging and liming the bedding material of the enclosures, and keeping the remaining partridges in an aerial aviary with a wire mesh floor prevented additional cases of histomoniasis.Discussion: In Brazil, as in other countries, the sanitary management practices applied in commercial chicken production reached high levels of technification. However, this is not the case in ornamental bird breeding systems, which may still suffer the impacts of diseases that are practically extinct in industrial chicken flocks. For both diseases, diagnosis was based on typical clinical signs and detection of the pathogens in association with characteristic pathological findings. The occurrence of mycoplasmosis and histomoniasis was associated with improper management practices at the farm; the main risk factors observed were a high turnover of birds, the absence of quarantine, the absence of basic health care, overcrowding and poor hygiene. The prevention of further cases of both diseases was mostly established with the application of basic sanitary measures, including vaccination and anthelmintic dosing, for mycoplasmosis and histomoniasis respectively. This report alerts bird keepers and avian veterinarians of the importance of establishing proper sanitary management in local ornamental bird flocks. Because some of the ornamental bird species that have been commercially propagated worldwide may be included in the list of threatened species, the findings described here also show that simple health care may promote the fight against extinctions.

The article presents the modern views of clinicians and geneticists on one of the most severe genetic disorders of skeletal and connective tissues - osteogenesis imperfecta. The review provided the literature data that showed the incidence rates, genetic heterogeneity of osteogenesis imperfecta, as well as the role of some proteins involved in the construction of bone tissue, as well as a clinical classification of the main types of the disorder. The authors described a clinical case: a girl with typical clinical and radiological manifestations of the rarest of all types of osteogenesis imperfecta - type II (perinatal-lethal, congenital osteogenesis imperfecta, Vrolik’s syndrome). The child’s diagnosis was verified by a parallel DNA sequence analysis which showed a heterozygous mutation in exon 29 (c.1966G&gt; A) of COL1A1 gene not previously described in the literature. It caused the substitution of glycine for serine at position 656. The role of antenatal diagnostics and the importance of medical genetic counselling of the family before planning the next pregnancy due to the existing risk of re-birth of a sick child is outlined. Due to the fact that majority of the patients with the most prognostically unfavourable type II osteogenesis imperfecta, as a rule, die in utero, the described case of observation of the girl with typical clinical and X-ray signs of the disorder for almost 3 months of postpartum period is extremely rare and highly indicative. The detection of the heterozygous mutation in exon 29 (c.1966G &gt; A) of COL1A1 gene by a parallel DNA sequence analysis which was not previously described in the literature gives an additional significance to the described observation.

A 17-year-old primigravid woman presented with Cushing's syndrome. Typical clinical symptoms and signs developed at the beginning of pregnancy. By week 17 of gestation, plasma cortisol diurnal rhythm was absent and there was a paradoxical increase in plasma cortisol after a 1-mg dexamethasone overnight suppression test. Basal urinary free cortisol was 10 times above the upper limit (in pregnancy) and ACTH levels were suppressed. The diagnosis of ACTH--independent Cushing's syndrome was established. MRI scans revealed normal adrenal and pituitary glands. To control hypercortisolism, the patient was treated with metyrapone. At 34 weeks of gestation, the patient developed preeclampsia and underwent caesarean section. A female infant weighing 1070 g was delivered. No apparent metyrapone-induced teratogenic effects were observed. Cushing's syndrome in the patient resolved within three weeks of delivery. No corticosteroid replacement therapy either for child or mother was needed. Eight months after delivery the patient became pregnant again and rapidly developed Cushing's syndrome with typical clinical symptoms and signs and laboratory results (urinary free cortisol 6464 nmol/24 h). This second pregnancy was unwanted and terminated by artificial abortion that was followed by rapid resolution of hypercortisolism. A third pregnancy, 12 months after delivery was also accompanied by the rapid development of hypercortisolism which recovered after artificial termination. The mechanisms by which pregnancy-induced Cushing's syndrome occurred in this patient are unclear. Aberrant responsiveness or hyperresponsiveness of adrenocortical cells to a non-ACTH and non-CRH substance produced in excess in pregnancy should be considered. Metyrapone suppression of hypercortisolism currently represents the best treatment for these rare cases.

BACKGROUNDThe EANO ESMO guidelines have proposed a classification of leptomeningeal metastases (LM) based on clinical (typical/atypical), cytological (positive/negative/equivocal) and MRI (A linear, B nodular, C linear and nodular, D normal or hydrocephalus only) presentation. Type I LM is defined by the presence of tumor cells in the cerebrospinal fluid (CSF) (confirmed LM) whereas type II LM is defined by typical clinical and MRI signs (probable or possible LM). Here we explored the clinical utility of these EANO ESMO LM subtypes.PATIENTS AND METHODSWe retrospectively assembled data from 254 patients with newly diagnosed LM from different solid tumors, including as main primary tumors breast cancer (n=98, 45%), lung cancer (n=65, 25.5%) and melanoma (n=51, 13.5%). Survival curves were estimated using the Kaplan-Meier method and compared by Log-rank test.RESULTSMedian age at LM diagnosis was 56.5 years (range 20–82 years). Typical clinical LM symptoms or signs were noted in 225 patients (88.5%); only 13 patients (5%) were clinically asymptomatic. The most common MRI subtype was A seen in 117 patients (46%). Types B (n=33, 13%), C (n=54, 21%) and D (n=50, 19.5%) were less common. Tumor cells were observed in the CSF in 186 patients (73%) whereas the CSF was equivocal in 24 (9.5%) and negative in 44 (17.5%) patients. Patients with confirmed LM had inferior outcome than patients with probable or possible LM (p=0.0063). Type I patients had inferior outcome than type II patients (p=0.0019). Nodular disease was a negative prognostic factor in type II LM, but not in type I LM (p=0.0138).CONCLUSIONThe presence of tumor cells in the CSF appears to have a greater prognostic role than the neuroimaging presentation. EANO ESMO LM subtypes are highly prognostic and should be considered in the design of clinical trials.

391O - Prognostic role of the EANO ESMO classification of leptomeningeal metastases

BACKGROUND The EANO ESMO guidelines have proposed a classification of leptomeningeal metastases (LM) based on clinical (typical/atypical), cytological (positive/negative/equivocal) and MRI (A linear, B nodular, C linear and nodular, D normal or hydrocephalus only) presentation. Type I LM is defined by the presence of tumor cells in the cerebrospinal fluid (CSF) (confirmed LM) whereas type II LM is defined by typical clinical and MRI signs (probable or possible LM). Here we explored the clinical utility of these EANO ESMO LM subtypes for choice of treatment and outcome. PATIENTS AND METHODS We retrospectively assembled data from 254 patients with newly diagnosed LM from different solid tumors, including as main primary tumors breast cancer (n=98, 45%), lung cancer (n=65, 25.5%) and melanoma (n=51, 13.5%). Survival curves were estimated using the Kaplan-Meier method and compared by Log-rank test. RESULTS Median age at LM diagnosis was 56.5 years (range 20-82 years). Typical clinical LM symptoms or signs were noted in 225 patients (88.5%); only 13 patients (5%) were clinically asymptomatic. The most common MRI subtype was A seen in 117 patients (46%). Types B (n=33, 13%), C (n=54, 21%) and D (n=50, 19.5%) were less common. Tumor cells in the CSF were observed in 186 patients (73%) whereas the CSF was equivocal in 24 (9.5%) and negative in 44 (17.5%) patients. Patients with confirmed LM had inferior outcome than patients with probable or possible LM (p=0.0063). Type I patients had inferior outcome than type II patients (p=0.0019). Nodular disease was a negative prognostic factor in type II LM, but not in type I LM (p=0.0138). CONCLUSION The EANO ESMO LM subtypes are highly prognostic and should be considered for stratification and overall design of clinical trials.

Typical and atypical clinical signs and symptoms of myocardial infarction and delayed seeking of professional care among blacks

Treatment of canine parvoviral enteritis with interferon-omega in a placebo-controlled challenge trial

The objective of this study was to characterize an outbreak of anthrax among animals in North Dakota in 2005, and determine characteristics and clinical signs associated with the disease. A total of 243 animals (183 cattle, 32 bison, 11 horses, 11 elk, five sheep and one deer) were diagnosed with anthrax at the Veterinary Diagnostic Laboratory at North Dakota State University, Fargo. Anthrax cases were defined as animals with typical clinical signs and positive results of laboratory culture and polymerase chain reaction (PCR) methods. Data for the study were obtained from veterinary laboratory records and questionnaires mailed to producers of affected animals. Anthrax occurred from July 1 to October 12 of 2005. The cases were located in 16 of 53 counties, specifically in eastern North Dakota, with Ransom, Lamoure and Barnes counties reporting most (71%) of the cases. The number of animals affected per premise varied from one to 40. The first cases were reported in bison. Males from all species infected had a higher attack rate (18/1000) than females (3/1000) with a gender ratio of 6:1, respectively. The predominant clinical signs in all cases were sudden death (38%) and bleeding from orifices (17%). Only 11 producers reported having vaccinated animals before the outbreak. Penicillin and tetracycline antibiotics were administered to animals during the outbreak. Forty producers (37%) burned and buried carcasses using commercial disposal services. Sixty-eight producers (63%) disposed of carcasses themselves by either burial only (11%), burned only (4.6%), or burned and buried (84.4%). Animals affected, clinical signs and final outcome were consistent with a natural anthrax outbreak.