In this clinical case, we are presented with a woman who rapidly presents dyspnea with hypoxemia, a picture compatible with pulmonary thromboembolism. The prothrombin time of 90% and the aPTT with a ratio of 2, is translating a coagulation problem; and antiphospholipid antibodies can be detected through the prolongation of phospholipid-dependent coagulation tests, correct answer 1. On the other hand, although factor V Leiden has been identified as a common cause of familial thrombosis, it would not alter the clotting time. In the case of hemophilia there would be a problem in blood coagulation but it is not a frequent cause of thromboembolism. Finally, although acute pericarditis could manifest itself in 4 days and with tachycardia, the rest of the symptoms or analytical parameters are not characteristic.

In this clinical case, we are presented with a woman who rapidly presents dyspnea with hypoxemia, a picture compatible with pulmonary thromboembolism. The prothrombin time of 90% and the aPTT with a ratio of 2, is translating a coagulation problem; and antiphospholipid antibodies can be detected through the prolongation of phospholipid-dependent coagulation tests, [HIDDEN]. On the other hand, although factor V Leiden has been identified as a common cause of familial thrombosis, it would not alter the clotting time. In the case of hemophilia there would be a problem in blood coagulation but it is not a frequent cause of thromboembolism. Finally, although acute pericarditis could manifest itself in 4 days and with tachycardia, the rest of the symptoms or analytical parameters are not characteristic.

A 45-year-old woman with no history of interest consults for dyspneic sensation of about 4 days of evolution. Examination shows rhythmic tachycardia, without murmurs and pulmonary auscultation is normal. Arterial blood gases showed a pO2 of 70 mmHg and a pCO2 of 32 mmHg. Hemogram, renal and hepatic function are normal. Prothrombin time 90%, activated partial thromboplastin time (APTT) ratio of 2 to control (N <1.2). Which of the following is the most likely diagnosis?

Case 294: Catastrophic Antiphospholipid Syndrome.

History A 50-year-old woman presented to the emergency department of our hospital with a 2-day history of lower limb pain associated with unusual asthenia and diffuse arthralgia over the past 3 weeks. She was a native of Guinea and had lived in France for most of her life, working as a personal care assistant. Her only medical history of note was an occurrence of fetal death at 12 weeks gestation when she was 35 years old. She had bilateral lower limb swelling, without changes in skin temperature or color. All proximal and distal arterial pulses were felt. General physical examination findings were otherwise unremarkable. Her laboratory tests showed a decreased hemoglobin concentration of 8.9 g/dL (normal range, 12-16 g/dL), a decreased platelet count of 45 × 10<sup9</sup/L (normal range, [150-400] × 10<sup9</sup/L), a C-reactive protein level of 158 mg/L (normal range, <5 mg/L), and a d-dimer level of 2000 mg/L (normal range, <500 mg/L]). Compression US of the lower limbs revealed bilateral calf vein thrombosis involving the fibular and posterior tibial veins. Curative anticoagulation using low-molecular-weight heparin (enoxaparin, subcutaneous injection of 100 units per kilogram of body weight twice a day) was started. The day after the start of anticoagulation therapy, the patient reported dyspnea and acute chest and abdominal pain. Her vital signs were assessed, and she had elevated blood pressure and increased heart rate and respiratory rate, but she remained afebrile. Her cardiac auscultation was unremarkable, besides tachycardia. Skin examination revealed small areas of necrosis on the fingertips of her right hand. Laboratory studies were repeated and showed an increase in serum creatinine level from a baseline value of 0.49 mg/dL to a new value of 1.01 mg/dL (normal range, 0.6-1.1 mg/dL), an apparition of low-grade proteinuria of 0.43 g per day (normal range, <0.3 g/ day), and a high serum troponin level of 1066 ng/L (normal range, <14 ng/L), whereas electrocardiography showed no ST segment modification and echocardiography revealed a moderately altered left ventricular ejection fraction (45%). There was no coronary occlusion seen at emergency coronarography. Contrast-enhanced CT of the chest, abdomen, and pelvis was performed (Figs 1, 2) together with cardiac MRI (Figs 3, 4).

[Catastrophic antiphospholipid syndrome and acute heart failure. Report of a case].

A 33 years old woman was admitted to the hospital after four days with cough, dyspnea, orthopnea and hemoptysis. Blood pressure was 170/90 mmHg, pulse was 112 and temperature was normal. She had cyanosis and a left ventricular gallop, without heart murmurs. A chest radiograph revealed pulmonary edema and echocardiogram showed a global left ventricular systolic disfunction. Oxygen and furosemide were started, but cardiopulmonary collapse ensued. The patient was supported with mechanical ventilation and treated with inotropic drugs. A right sided cardiac catheterization showed pulmonary wedge pressure of 18 mmHg and a cardiac index of 3 l/min/m2. The levels of creatinine and urea nitrogen were elevated and a urine protein was 97 mg/dl. Coagulation tests were normal except by a positive lupic anticoagulant. Markers of connective tissue diseases or vasculitis were negatives. The clinical evolution suggested that a catastrophic antiphospholipid syndrome was ongoing. Intravenous corticoids, gammaglobulin and cyclophosphamide were administered with transient improvement. On her fourth day of treatment, the patient presented sudden pulmonary bleeding and embolism. A plasmapheresis was performed with improvement of renal, cardiac and pulmonary function. After this episode, the patient has been treated with prednisone and oral anticoagulants treatment for the last two years, without further clinical events.

[Pulmonary embolism in a girl with nephrotic syndrome and factor V Leiden - case report].

Thromboembolic complications are found in 2-3% of children with nephrotic syndrome (NS); this increased risk is caused by hypovolemia, hemoconcentration, increased number and activity of platelets, hyperfibrinogenemia and loss of coagulation inhibitors. Risk is even higher in case of additional factors e.g. congenital thrombophilia. Girl with NS aged 17 11/12 years was admitted to hospital due to respiratory tract infection with cough and back pain. NS started 9 months earlier and she had two bouts of disease, and was treated only with prednisone (current dose - 60 mg/48h). On admission she was without any abnormalities on auscultation, with BP 111/65 mmHg, HR 80 bpm, satO2 99%. Lab results showed the increase of WBC 18.3×103/μL, D-dimers 23038 μg/L and proteinuria 900 mg/dL. Other values of examined parameters were in normal limits. Chest X-ray and ECG were also normal. Presumptive diagnosis of pulmonary embolism was made and the patient was given 1000IU of antithrombin III and nadroparine (2x90IU/kg/24h s.c.). In ECHO the occlusion of left pulmonary artery and preserved blood flow in right were revealed. In angioCT clot nearly filling lumen of left pulmonary artery, clot in intermediate part of right pulmonary artery, and focus of pulmonary infarction in 10th segment of left lung were found. Doppler USG of lower limb veins did not reveal thrombi or perforator vein incompetence. Treatment with nadroparine was continued, and rapid improvement of clinical condition and disappearance of pain and cough were observed. Mycophenolate mofetil was added, which resulted in subsidence of proteinuria. Rivaroxaban was used in prophylaxis of recurrences of thromboembolism. Tests for thrombophilia revealed factor V Leiden in patient.

Pulmonary hypertension secondary to hyperviscosity in a patient with rheumatoid arthritis and acquired von Willebrand disease: a case report.

Acquired von Willebrand disease is initiated by autoantibodies and hyperviscosity syndrome caused by a massive polyclonal hypergammaglobulinemia. Acquired von Willebrand disease associated with autoimmune disease in addition to pulmonary hypertension during emergency room presentation is a rare condition. To the best of our knowledge, this is the second case reported in the literature treated with success; the first one was reported in 1987. A 28-year-old mestizo man with a 3-year history of inflammatory arthritis was admitted to our hospital. An overlap of rheumatoid arthritis with systemic lupus erythematosus was suspected; therefore methotrexate was initiated, and later changed to leflunomide because of liver toxicity. Prothrombin time, international normalized ratio and activated partial thromboplastin times were normal (11/10.4 seconds; 1.2; 31.1/26.9 seconds, respectively), von Willebrand factor activity was observed with low ristocetin cofactor at 33.6UI/dL, high von Willebrand factor antigen >200UI/dL, and a low von Willebrand factor: ristocetin cofactor to von Willebrand factor antigen ratio. He was admitted to the emergency room with a 24-hour evolution of progressive dyspnea, cough, thoracic pain, and palpitations, 104 beats/min, 60/40 mmHg, temperature of 38°C, pulse oximetric saturation 88% and 30 breaths/minute. Cold, pale and mottled skin was also observed. He was then transferred to the intensive care unit. The placement of a pulmonary artery catheter was made. The initial patterns showed a precapillary pulmonary hypertension; acute pulmonary embolism was the first choice for diagnosis. Pulmonary angiography was conducted, and when no clot was discovered, pulmonary artery hypertension associated with connective tissue disease was considered. Serum protein electrophoresis confirmed the presence of a massive polyclonal hypergammaglobulinemia, and no paraproteinemia or monoclonal cell population was found from the electrophoretic pattern of the patient's plasma. Hypergammaglobulinemia was the cause of hyperviscosity syndrome associated with autoantibodies. Three sessions of plasma exchange therapy were made, and clinical improvement was observed. He was then discharged from the intensive care unit and hospital, respectively. He is now attended by an external consult and has no respiratory symptomatology. Hyperviscosity syndrome with pulmonary arterial hypertension presentation in a patient with acquired von Willebrand disease in an autoimmune context is a rare condition that can be treated successfully with plasmapheresis and critical care support.

A 2-year-old boy with circulatory failure owing to streptococcal toxic shock syndrome: case report.

A 2-year-old boy presented with severe hypotension and acute kidney injury after a prodrome of non-bloody diarrhoea and fever in the preceding 3 days. He had a mild Ebstein cardiac anomaly but otherwise a normal past history and growth. On examination, he looked ill, his temperature was 37.5 °C, circulation was poor, and there were several purpuric lesions on the face, hands and scrotum. Haemoglobin was 7.8 g/dL (11-14), total white cell count 27 × 10<sup9</sup/L, platelets 62 × 10<sup9</sup/L, blood urea nitrogen 20.7 mmol/L (4.2-17.1), serum creatinine 95.4 μmol/L (21.2-36.2), CRP 154 mg/L (<5), AST 296 U/L (11-50), ALT 909 U/L (7-40) and C<sub3</sub component of complement 0.8 g/L (0.9-1.8). Activated partial thromboplastin time (APTT) and prothrombin time (PT) were prolonged and fibrinogen level was 1.0 g/L (2-4). He received immediate fluid resuscitation (IV 0.9% saline solution, 2 × 10 ml/kg boluses, followed by glucose 5/0.45% sodium chloride solution, 2 × 10 ml/kg) and antibiotics (ciprofloxacin and amikacin) but circulation continued to deteriorate with development of decreased consciousness. He was placed on mechanical ventilation and vasopressor agents were added. Despite improved circulation over the next 2 days, he developed oliguria, progressive fluid overload, generalised oedema and a right-sided pleural effusion. Dialysis was commenced on day 3 of admission. Differential diagnosis included sepsis, atypical haemolytic uraemic syndrome and lupus nephritis. Blood and urine cultures remained negative but an anti-streptolysin O titre of 1318 (<200) IU/mL led to the diagnosis of streptococcal toxic shock syndrome which is rare in early childhood and associated with high mortality. Haemodialysis was commenced and continued for 10 days with successful treatment of fluid overload and subsequent extubation. Renal function was completely restored over the following 6 weeks and he was discharged in good clinical condition about 2 months after intial admission. The clinical course and outcome are discussed, and the importance of timely initiation of dialysis when there is fluid overload is emphasised.

Brodifacoum

In another case reported in 2013, a 48-year-old female patient reported 4 days of mild dyspnea, dry cough, bilateral popliteal fossae pain, and diffuse upper abdominal pain. She had no history of liver disease or alcohol or illicit substance abuse. Initial physical examination was remarkable only for mildly pale conjunctivae and mild abdominal tenderness and pain in the left popliteal fossa. A complete blood count and complete metabolic panel were normal. Prothrombin time (PT) was above 100 s, partial thromboplastin time (PTT) was above 200 s and international normalized ratio (INR) was reported as above 12.0. Urinalysis revealed hematuria (blood in the urine). Venous Doppler ultrasound of lower extremities demonstrated left popliteal vein thrombosis. Computed tomography scan of the abdomen demonstrated transmural hematoma, and a fecal occult blood test was positive. A full anticoagulant work-up showed critical reduction of vitamin K-dependent factors II, VII, IX, and X. PT and PTT

[Metastatic prostate cancer complicated with chronic disseminated intravascular coagulopathy causing acute renal failure, mimicking thrombotic thrombocytopenic purpura and hemolytic uremic syndrome: pathomechanism, differential diagnosis and therapy related to a case].

Disseminated intravascular coagulopathy (DIC) is characterized as activation of the clotting system resulting in fibrin thrombi, gradually diminishing levels of clotting factors with increased risk of bleeding. Basically two types of DIC are distinguished: (1) chronic (compensated) - with alteration of laboratory values and (2) acute (non-compensated) - with severe clinical manifestations: bleeding, shock, acute renal failure (ARF), transient focal neurologic deficit, delirium or coma. Chronic DIC related to metastatic neoplasia is caused by pancreatic, gastric or prostatic carcinoma in most of the cases. Incidence rate of DIC is 13-30% in prostate cancer, among those only 0.4-1.65% of patients had clinical signs and symptoms of DIC. In other words, chronic DIC is developed in one of eight patients with prostate cancer. DIC is considered as a poor prognostic factor in prostatic carcinoma. The similar clinical and laboratory findings of TTP-HUS (thrombotic thrombocytopenic purpura - hemolytic uremic syndrome) and DIC makes it difficult to differentiate between them. A 71 years old male patient with known chronic obstructive pulmonary disease, benign prostatic hyperplasia, significant carotid artery stenosis, gastric ulcer and alcoholic liver disease was admitted to another hospital with melena. Gastroscopy revealed intact gastric mucosa and actually non-bleeding duodenal ulcer covered by clots. Laboratory results showed hyperkalemia, elevated kidney function tests, indirect hyperbilirubinemia, increased liver function tests, leukocytosis, anemia, thrombocytopenia and elevated international normalized ratio (INR). He was treated with saline infusions, four units of red blood cells and one unit of fresh frozen plasma transfusions. Four days later he was transported to our Institution with ARF. Physical examination revealed dyspnoe, petechiae, hemoptoe, oliguria, chest-wall pain and aggressive behavior. Thrombocytopenia, signs of MAHA (fragmentocytes and helmet cells in the peripheral blood), normal INR, elevated lactate dehydrogenase (LDH) and ARF suggested TTP-HUS. Hemodialysis and six plasmaferesis (PF) were carried out. After the fifth PF, skin manifestations of thrombotic microangiopathy occurred on the feet. Clotting analysis revealed elevated D-dimer (>5 μg/mL), normal fibrinogen (3.2 g/L), a slightly raised INR (1.36) and activated partial prothrombin time (APTT) (45.8 sec), normal reticulocyte (57 G/L) and a slightly low platelet count (123 G/L), which proved to be chronic DIC. Therapeutic dose of low-molecular-weight heparin (LMWH) was started. Elevated prostate-specific antigen (PSA) (109.6 ng/mL) suggested prostatic carcinoma. Prostate biopsy revealed adenocarcinoma (Gleason: 4+4 for left lobe and 3+3 for right lobe). Elevated alkaline phosphatase suggested metastases in the bone, which were confirmed by bone scintigraphy. Combined androgen blockade (CAB) was started. After three months follow-up our patient's status is satisfactory. PSA is in the normal range (4.6 ng/mL). Thrombocytopenia of uncertain origin with normal or raised INR, APTT, elevated D-dimer, normal fibrinogen and reticulocyte count prove the diagnosis of chronic DIC. This process warrants searching for metastatic neoplasia. Due to the relatively low serum levels of circulating procoagulant factors (e.g. tissue factor), therapeutic dose of LMWH can be used with good efficiency in chronic DIC with low risk of bleeding. Severe DIC as a complication of metastatic prostate cancer can be treated by androgen deprivation therapy (ADT) or CAB in combination with ketokonazole and concomitant use of supportive treatment. Deme D, Ragán M, Kovács L, Kalmár K, Varga E, Varga T, Rakonczai E. Metastatic prostate cancer complicated with chronic disseminated intravascular coagulopathy causing acute renal failure mimicking thrombotic thrombocytopenic purpura and hemolytic uremic syndrome: pathomechanism, differential diagnosis and therapy related to a case.

Thrombophilia

Diagnosis Tests for thrombophilia include complete blood count (with examination of the blood film), prothrombin time, partial thromboplastin time, thrombodynamics test, thrombin time and reptilase time, lupus anticoagulant, anti-cardiolipin antibody, anti-β2 glycoprotein 1 antibody, activated protein C resistance, fibrinogen tests, factor V Leiden and prothrombin mutation, and basal homocysteine levels. Testing may be more or less extensive depending on clinical judgement and abnormalities detected on initial evaluation. For hereditary cases, the patient must have at least two abnormal tests plus family history.

Von Willebrand disease

Diagnosis Basic tests performed in any patient with bleeding problems are a complete blood count-CBC (especially platelet counts), activated partial thromboplastin time-APTT, prothrombin time with International Normalized Ratio-PTINR, thrombin time-TT, and fibrinogen level. Patients with abnormal tests typically undergo further testing for hemophilias. Other coagulation factor assays may be performed depending on the results of a coagulation screen. Patients with von Willebrand disease typically display a normal prothrombin time and a variable prolongation of partial thromboplastin time.

An unusual cause of acute abdominal pain - a case presentation.

In 1983, Graham Hughes described a condition of Antiphospholipid Syndrome in which there was a danger of thrombosis. The condition is readily detectable by blood tests and, once diagnosed; the risk of further thrombosis can be significantly reduced by anticoagulation treatments. Affected groups of patients can be distinguished by a specific blood test - the detection of antiphospholipid antibody (Ref-1). Patients with Hughes syndrome have hypercoaguable state with a markedly increased risk of both arterial and venous thrombosis and there is temporal persistence of antibody positivity. A 44-year-old woman was admitted under the acute surgical "take" with left sided abdominal pain radiating to her back. She had a history of borderline thyrotoxicosis in the early 1990s. She was on etonogestrel-releasing implants for contraception and there was no history of previous deep venous thrombosis. She was very tender, locally, over the left side of the abdomen. Investigations showed haemoglobin of 13.2 g/dl, white cell count of 19.9 10*9/L, and platelets 214 10*9/L with neutrophilia. Amylase and renal function tests were found to be normal. Liver function tests were deranged with Gamma GT 244 u/l (twice normal). An abdominal Ultrasound Scan suggested a possible splenic infarction, which was confirmed by a CT scan of her abdomen. Tests were carried out to investigate the possibility of a post thrombotic state. Coagulation risk factors for thrombosis were within the normal limits; Protein S 67 %(60-140), Protein C 103 % (72-146), Antithrombin 3 110 %(80-120) and Activated P C Resistance was 1.9(2.0-4.3). The Hams test was negative but the Anticardiolipin antibody test was positive. IgM level was 52 (normal is up to 10) and IgG was 18.8 (normal is up to 10). She also had border line APC Sensitivity 1.9 (2 to 4.3). Kaolin time 49 sec (70-120) Ktmix 64 sec (70-120), thyroid function test revealed TSH 0.32 micro/L, fT4 20.2 pmol/L (10-25). Subsequent determination of Anticardiolipin antibody was negative. Her symptoms were settled with the use of simple analgesia and she was discharged home with long-term anticoagulation medication. The INR target for long-term anticoagulation was aimed at >3. This case presented to us as an acute abdominal pain. Subsequent investigations revealed the presence of splenic infarction. Coagulation risk factors for thrombosis proved negative. Haematological investigations revealed the presence of anticardiolipin antibodies at the first instance but subsequent determinations were negative. Hence, it mimicked Hughes syndrome initially but the criteria for temporal persistence of anticardiolipin antibody was not fulfilled. Unusual surgical presentation of a thrombotic abnormality as abdominal pain due to splenic infarction.

Acquired haemophilia

Diagnosis Any acute or recent onset of bleeding symptoms in a patient with no previous history of bleeding, especially in elderly or post-partum patients, and an unexplained isolated prolonged activated partial thromboplastin time (aPTT) suggest the diagnosis of AHA, and need further investigation. The differential diagnosis in prolonged aPPT with a normal prothrombin time (PT) includes factor deficiencies, lupus anticoagulant or heparin therapy. The first step to distinguish between factor deficiency and the presence of an inhibitory substance is to perform a mixing test, in which patient plasma and normal plasma are mixed and aPTT measured; correction of prolonged aPTT suggests a factor deficiency while persistent prolongation indicates the presence of an inhibitor. Prolongation of the aPTT in a mixture of patient and normal plasma after a 1-2 h incubation compared to an immediate mix is typical of FVIII autoantibodies, as FVIII inhibitors are time and temperature-dependent.

Coagulation

Assessment Numerous tests are used to assess the function of the coagulation system: Common: aPTT, PT (also used to determine INR), fibrinogen testing (often by the Clauss method), platelet count, platelet function testing (often by PFA-100), thrombodynamics test. Other: TCT, bleeding time, mixing test (whether an abnormality corrects if the patient's plasma is mixed with normal plasma), coagulation factor assays, antiphospholipid antibodies, D-dimer, genetic tests (e.g. factor V Leiden, prothrombin mutation G20210A), dilute Russell's viper venom time (dRVVT), miscellaneous platelet function tests, thromboelastography (TEG or Sonoclot), euglobulin lysis time (ELT). The contact activation (intrinsic) pathway is initiated by activation of the "contact factors" of plasma, and can be measured by the activated partial thromboplastin time (aPTT) test.

Case 294.

History A 50-year-old woman presented to the emergency department of our hospital with a 2-day history of lower limb pain associated with unusual asthenia and diffuse arthralgia over the past 3 weeks. She was a native of Guinea and had lived in France for most of her life, working as a personal care assistant. Her only medical history of note was an occurrence of fetal death at 12 weeks gestation when she was 35 years old. She had bilateral lower limb swelling, without changes in skin temperature or color. All proximal and distal arterial pulses were felt. General physical examination findings were otherwise unremarkable. Her laboratory tests showed a decreased hemoglobin concentration of 8.9 g/dL (normal range, 12-16 g/dL), a decreased platelet count of 45 × 10<sup9</sup/L (normal range, 150-400 × 10<sup9</sup/L), a C-reactive protein level of 158 mg/L (normal range, <5 mg/L) and a d-dimer level of 2000 mg/L (normal range, <500 mg/L). Compression US of the lower limbs revealed bilateral calf vein thrombosis involving the fibular and posterior tibial veins. Curative anticoagulation using low-molecular-weight heparin (enoxaparin, subcutaneous injection of 100 units per kilogram of body weight twice a day) was started. The day after the start of anticoagulation therapy, the patient reported dyspnea and acute chest and abdominal pain. Her vital signs were assessed, and she had elevated blood pressure and increased heart rate and respiratory rate, but she remained afebrile. Her cardiac auscultation was unremarkable, besides tachycardia. Skin examination revealed small areas of necrosis on the fingertips of her right hand. Laboratory studies were repeated and showed an increase in serum creatinine level from a baseline value of 0.49 mg/dL to a new value of 1.01 mg/dL (normal range, 0.6-1.1 mg/dL), an apparition of low-grade proteinuria of 0.43 g per day (normal range, <0.3 g/day), and a high serum troponin level of 1066 ng/L (normal range, <14 ng/L), whereas electrocardiography showed no ST segment modification and echocardiography revealed a moderately altered left ventricular ejection fraction (45%). There was no coronary occlusion seen at emergency coronarography. Contrast-enhanced CT of the chest, abdomen, and pelvis was performed (Figs 1, 2) together with cardiac MRI (Figs 3, 4).

Activated protein C resistance phenotype in patients with antiphospholipid antibodies.

The effect of antiphospholipid antibodies (aPL) on the action of activated protein C (APC) was examined in 32 patients: 19 with lupus anticoagulant (LA), 6 with anticardiolipin antibodies (aCL), and 7 with LA and aCL. Eighteen patients had a ratio of activated partial thromboplastin time (APTT) with APC to APTT without APC (APTT ratio) <2.06 (cut-off level) and no factor V Leiden mutation; these patients showed APC-resistance (APC-R) phenotype. The mean prolongation of APTT after addition of APC in a control group was 45.3 seconds, with a lower limit of 31.4 seconds. Only 3 of the 18 patients with low APTT ratio had a prolongation of <31.4 seconds; they were classified as true APC-R phenotype, whereas the other 15 patients were classified as spurious APC-R. Of the 3 patients with true APC-R, 2 had deep venous thrombosis, 1 with pulmonary embolism, and the third had recurrent abortion. Of the other 15 patients, 2 had had ischemic stroke, 1 had recurrent abortion, and 12 were asymptomatic. Circulating APC level was measured in 14 of the 18 aPL patients with a low APTT ratio; it was lower than the normal lower limit in 4 patients and within the lower limit in 2. Three of the 4 patients with reduced APC levels had a history of thrombosis. We conclude that patients with aPL who show APC-R phenotype due to a low APTT ratio without the factor V Leiden mutation can be classified into two groups: true and spurious APC-R phenotype. Since those with true APC-R phenotype could have greater thrombotic risk, adequate classification of these patients is important. Moreover, aPL can sometimes interfere with the activation of protein C, thus reducing the circulating levels of APC, and this could constitute another thrombotic risk factor.

Treatment of massive pulmonary thromboembolism with low intrapulmonary dosages of urokinase. Short-term angiographic and hemodynamic evolution.

Sixteen patients who had massive pulmonary thromboembolism and shock had no history of cardiopulmonary disease. We present an evaluation of the short-term effects of fibrinolytic treatment consisting of intrapulmonary administration of a bolus of 500,000 IU of urokinase followed by infusion of 1 x 10(6) IU into the right auricle over 12 h and subsequent intravenous infusion of heparin. For each patient, the effectiveness of treatment was evaluated by comparing pretreatment angiographic and hemodynamic parameters with those measured 48 h after the start of treatment. The Miller index fell from 22.9 +/- 5.9 to 9.8 +/- 3.3 (p less than 0.001), with a mean improvement of 57.2 percent. All the hemodynamic parameters studied (cardiac output and index, total pulmonary vascular resistance, and systolic, diastolic, and mean pulmonary vascular pressure) also exhibited statistically significant differences between pretreatment and posttreatment values (p less than 0.001 for each parameter), with a mean improvement of over 30 percent in each case. All the patients survived, and in no case did treatment fail; only one patient (6.2 percent) suffered severe hemorrhage. We conclude that this form of administration of urokinase is useful for patients with critical massive pulmonary thromboembolism.

Prothrombin time

The prothrombin time (PT) – along with its derived measures of prothrombin ratio (PR) and international normalized ratio (INR) – is an assay for evaluating the extrinsic pathway and common pathway of coagulation. This blood test is also called protime INR and PT/INR. They are used to determine the clotting tendency of blood, in such things as the measure of warfarin dosage, liver damage, and vitamin K status. PT measures the following coagulation factors: I (fibrinogen), II (prothrombin), V (proaccelerin), VII (proconvertin), and X (Stuart–Prower factor). PT is often used in conjunction with the activated partial thromboplastin time (aPTT) which measures the intrinsic pathway and common pathway of coagulation. Laboratory measurement

[Relative value of different antiphospholipid antibodies detected in a department of internal medicine: retrospective study of 124 patients].

The value of antiphospholipid antibodies (aPL) detected in the sera of the patients of an Internal Medicine department is not univocal and is still much debated. To test the contribution of such new markers, we reviewed the records of patients having antiphospholipid antibodies detected between 1996 and 1997. One hundred and twenty four patients, having at least one of these two aPL: lupus anticoagulant (LA), anticardiolipin antibodies (aCL), or one of these two anti-proteins: anti-beta 2glycoprotéin I antibodies (anti-beta 2GPI) or anti-prothrombin antibodies (aPT), were studied. LA was detected by a PTT-LA technique and aCL, anti-beta 2GPI and aPT by ELISA-sandwich techniques. For each patient we recorded sex, age, personal and familial history of thrombosis, fetal losses and systemic disease, the reason of aPL detection, the final diagnosis, activated partial thromboplastin time (aPTT), platelets count and type of aPL. The population was composed of 77 women (62%) and 47 men (38%) with a mean age of 54 years [12-92 years]. A thrombocytopenia was strongly correlated to aCL presence (OR = 6.15 et p = 0.03). The reason of aPL detection was venous thrombosis, recurrent fetal losses, systemic disease, infectious disease or fortuitous discovery of a prolonged aPTT. The final diagnosis was a systemic disease in 57% of cases, an infectious disease in 14.5%, a thrombosis in 4.5% and a neoplasia in 3%. LA was detected in 54% of patients, aCL in 39.5%, anti-beta 2GPI in 23% and aPT in 31%. No relationship between the aPTT value and the type of aPL could be established. Our study shows that familial histories of venous thrombosis or systemic disease are useful to enhance antiphospholipid antibodies detection; that LA is mostly associated to systemic and infectious diseases; that aCL and anti-beta 2GPI are predominant in case of venous thrombosis and that thrombocytopenia has to enhance aCL detection and the discussion about a possible APS.

Acquired hemophilia: clinical case of hemorrhage caused by inhibitors against factor VIII.

Acquired hemophilia is caused by antibodies against coagulation factors, especially against factor VIII. As it is a low prevalence disease, our objective is to present an idiopathic case of acquired hemophilia to facilitate decision-making in clinical practice for others, exposing the therapeutic modality used. 65 years old woman, started with non-trauma hematomas, with asthenia, adynamia and dyspnea. Laboratory studies showed anemia (hemoglobin 7.1 g/dl, hematocrit 21%, mean corpuscular volume 91 fl, mean corpuscular hemoglobin 29.6 pg) and long clotting times (activated partial thromboplastin time 100 seconds) and with prothrombin time and International Normalized Index (17 seconds and 1.2 seconds respectively). So, plasma dilution tests were performed with plasma, without aPTT correction (1:2, 76.6 seconds; 1: 4, 60 seconds; 1: 8, 45 seconds) evidencing the presence of the inhibitor. The diagnosis was confirmed by the decrease in factor VIII (1%) and the presence of the factor VIII inhibitor (256 UB). The treatment started with prednisone and cyclophosphamide. Due to the presence of severe bleeding, treatment with activated prothrombin complex concentrate (CCpa) was required. Subsequently, Rituximab was prescribed, with clinical improvement and increased levels of hgb and reduced aPTT from the first week of treatment. The approach of acquired hemophilia should include control of the bleeding, the search for the etiology ruling out of the main causes of malignant neoplasms according to age and gender, and the immediate initiation of immunosuppression to decrease inhibitor levels.

Preserve encephalus in surgery of trauma: online survey. (P.E.S.T.O).

Traumatic brain injury (TBI) is a global health problem. Extracranial hemorrhagic lesions needing emergency surgery adversely affect the outcome of TBI. We conducted an international survey regarding the acute phase management practices in TBI polytrauma patients. A questionnaire was available on the World Society of Emergency Surgery website between December 2017 and February 2018. The main endpoints were the evaluation of (1) intracranial pressure (ICP) monitoring during extracranial emergency surgery (EES), (2) hemodynamic management without ICP monitoring during EES, (3) coagulation management, and (4) utilization of simultaneous multisystem surgery (SMS). The respondents were 122 representing 105 trauma centers worldwide. ICP monitoring was utilized in 10-30% of patients at risk of intracranial hypertension (IH) undergoing EES from about a third of the respondents [<in</i = 35 (29%)]. The respondents reported that the safest values of systolic blood pressure during EES in patients at risk of IH were 90-100 mmHg [<in</i = 35 (29%)] and 100-110 mmHg [<in</i = 35 (29%)]. The safest values of mean arterial pressure during EES in patients at risk of IH were > 70 mmHg [<in</i = 44 (36%)] and > 80 mmHg [<in</i = 32 (26%)]. Regarding ICP placement, a large percentage of respondents considered a platelet (PLT) count > 50,000/mm<sup3</sup [<in</i = 57 (47%)] and a prothrombin time (PT)/activated partial thromboplastin time (aPTT) < 1.5 times the normal control [<in</i = 73 (60%)] to be the safest parameters. For craniotomy, the majority of respondents considered PLT count > 100,000/mm<sup3</sup [<in</i = 67 (55%)] and a PT/aPTT < 1.5 times the normal control [<in</i = 76 (62%)] to be the safest parameters. Almost half of the respondents [<in</i = 53 (43%)], reported that they transfused red blood cells (RBCs)/plasma (P)/PLTs at a ratio of 1/1/1 in TBI polytrauma patients. SMS was performed in 5-19% of patients, requiring both an emergency neurosurgical operation and EES, by almost half of the respondents [<in</i = 49 (40%)]. A great variability in practices during the acute phase management of polytrauma patients with severe TBI was identified. These findings may be helpful for future investigations and educational purposes.

[Long-term anticoagulant therapy in subjects over 75 years of age. 100 cases].

100 patients (median age 79 years) were given anticoagulant therapy (ACT) for a period of time averaging 5 years 3 months (522 follow-up years).--Out of 3 522 Quick tests, converted into prothrombin times and all carried out in the same laboratory, the prothrombin time was at or less than 32% in 60.5%, and 34% in 69.6% of the tests.--The mean therapeutic doses were less than 27% of those for adults, and were decreased by 3 mg of phenindione per year over the age of 75, only the actively treated cases being retained.--The risks are the same as those for the middle-aged adult. They depend more on the quality of the investigations than upon age. In the group which has been studied, slight or frank haemorrhagic complications (0.05/year/patient) were the result of a demonstrable overdosage in only one case in four. They were not responsable for any deaths in this series.--because of the referral patterns, the patients studied consisted of 79 with ischaemic heart disease, 27 with peripheral vascular disease, 9 cerebrovascular accidents, and 6 with thrombo-emoblic problems, not counting the 23 complications during the course of the study. In those patients with ischaemic heart disease, well-regulated anticoagulant treatment was associated with a favourable clinical course, and the correlation was significant.--there is not argument against the administering of a full and prolonged course of ACT to a patient of more than 75 years of age.

Diagnostic analysis of lupus anticoagulant using clot waveform analysis in activated partial thromboplastin time prolonged cases: A retrospective analysis.

Hemophilia was diagnosed in precedence research of clot waveform analysis (CWA) using the activated partial thromboplastin time (APTT). In patients with antiphospholipid syndrome (APS), lupus anticoagulant (LA) causes an increase in APTT, suggesting that the waveform would probably be distorted. Therefore, we evaluated using clinical samples. CWA may be useful low cost for clinical detection of LA. We assessed the clinical value of CWA for detection of LA and coagulation using clinical blood samples collected from patients with a prolonged APTT. We used patient samples inspected between April 2011 and March 2013 in Yamagata University Hospital. CWA was performed using the ACL TOP coagulation analyzer, and the associated software program was used to calculate APTT clotting endpoints. An atypical peak was defined as a derivative plot that did not conform to the normal S-shaped clot reaction curve. In total, 162 patients, including 66 men and 96 women, with an average age of 46 years (range: 24-89 years) were included. We also collected control samples from unmatched healthy donors. All 162 patients were divided according to medication history or condition into the following five groups: heparin (n = 20), warfarin (n = 23), hepatic dysfunction (n = 13), normal (n = 20), and LA-positive antiphospholipid syndrome (APS; n = 86). Twenty healthy individuals were included as controls.Eighty patients had an atypical peak. Among all, 78 patients (90.6%) were LA-positive, and 2 patients (2.5%) were treated with warfarin. The remaining two patients had prothrombin time international normalized ratios (PT-INR) >4.0 while taking warfarin. Those who were APS LA positive with thrombosis and without thrombosis had split the reaction of clotting time, deceleration/acceleration time (D/A) ratio of 2.36 (1.99,3.24) vs 2.34 (2.04,2.86), respectively. The significant atypical peak and D/A ratio extension may be explained by the clotting waveforms observed specifically in patients with LA-positive APS.

[Catastrophic antiphospholipid syndrome and rituximab: a new report].

Catastrophic antiphospholipid syndrome is a distinctly rare dramatic condition characterized by widespread thrombosis of small vessels. Early diagnosis and aggressive therapies are essential in this condition because of its extremely high mortality rate. Therapeutic management include heparine, high dose steroids, cyclophosphamide, plasma exchange, intravenous immunoglobuline, however a number of patients are refractory to treatment. We review and discuss alternative and emerging treatment options by rituximab for patients who fail or cannot tolerate conventional therapy. A 36-year-old female with a two mounths history of dyspnea, palpitation and chest pain was admitted. Physical examination upon admission revealed a fever, ischemic digital necrosis, scleroderma of the hands and beaking of the nose. Laboratory tests showed normal level of liver enzymes, elevation of creatinine level, lymphopenia, haemolytic anaemia with negative Coombs tests, low platelet count, prolonged partial thromboplastin time. The D-Dimer value was 158 ng/ml. Urinalysis revealed a proteinuria. Antinuclear antibody tests and lupus anticoagulant were strongly positive. Echocardiography revealed severe pulmonary hypertension and pericarditis. There was no pulmonary embolism on thoracic angio tomodensitometry. The diagnosis of catastrophic antiphospholipid antibody syndrome associated with systemic lupus and scleroderma was established. She was treated with anticoagulants, corticotherapy, one pulse of intravenous cyclophosphamide, 2 doses of intravenous immunoglobuline and 5 sessions of plasmapheresis. Because of lack of response 2 doses of 375 mg weekly rituximab i.v. were added but she developed pulmonary embolism, alveolar haemorrhage and she died. Effectiveness of Rituximab for the CSAPL should be demonstrated by further studies.

[Splenic infarction caused by paradoxical emboli in severe pulmonary hypertension].

A 55-year-old woman developed increasing shortness of breath and breath-independent pain in the left lower chest. 20 years previously she had had an episode of pulmonary embolism and 10 years previously a central venous thrombosis in the left eye. No cause of the increased thrombogenesis had been found. On admission she had resting dyspnoea but a stable circulation. On auscultation the breath sounds were diminished over the left base and there was a diastolic murmur over the pulmonary area with an accentuated second sound. There was also marked tenderness below the left costal margin. Recurrent pulmonary embolism or left-sided pleuropneumonia was suspected. Arterial blood gases (without additional oxygen) showed severe hypoxaemia (pO2 42.3 mm Hg, pCO2 27.8 mm Hg, pH 7.455, oxygen saturation 80.5%). Transthoracic and transoesophageal echocardiography showed normal left ventricular dimensions, right atrial and ventricular dilatation, and an atrial septal aneurysm with a right to left interatrial shunt. Right heart catheterisation demonstrated severe pulmonary hypertension. Sonography, computed tomography and scintigraphy revealed multiple splenic infarcts. Heparinisation was instituted (partial thromboplastin time 70-90 s) and overlapping oral anticoagulation to a Quick value of 20%. Subsequently the calcium antagonist felodipine (15 mg daily) was given. The mean pulmonary artery pressure was 61 mm Hg before and 57 mm Hg after treatment. Splenic infarction resulting from paradoxical embolisation is rare, but should be routinely considered in the presence of thromboembolic phenomena.

Case 290.

History A 26-year-old man presented with a 1-month history of chest pain, a palpable and painful right inguinal mass, and edema in the right lower extremity. One month earlier, he started to experience left chest pain with no cough. Pulmonary CT angiography (CTA) revealed a left lower lobe segmental pulmonary embolus. The local hospital made a diagnosis of pulmonary embolism (PE). He received anticoagulants, and his chest pain was gradually relieved. At the time of current presentation, the patient was experiencing right lower extremity swelling and pain. Physical examination revealed a 4 × 3 cm palpable right inguinal mass with no redness. His medical history and family history were negative. The results of laboratory work-up were normal, with a D-dimer level of 0.16 mg/L fibrinogen equivalent units (reference range, <0.46 mg/L) and an international normalized ratio of 2.45 (therapeutic range, 2.0-3.0 for a patient taking warfarin), except the prothrombin time was 28.2 seconds (reference range, 9.6-12.8 seconds) and the activated partial thromboplastin time was 52.2 seconds (reference range, 24.8-33.8 seconds). Echocardiography, chest radiography, chest CT, and contrast-enhanced CT revealed no abnormalities. The patient underwent right lower extremity vascular conventional US (Philips IU22; Philips) with an L9-3 probe (3-9 MHz, venous condition) and contrast-enhanced US (1.5-2.0 mL, SonoVue; Bracco) with an intravenous bolus injection at the initial evaluation. Two days later, noncontrast and contrast-enhanced CT images of the lower abdomen (1.5 mL per kilogram of body weight, 300 mg/mL iomeprol, Iomeron; Bracco) were acquired for further evaluation (Figs 1-3).

First Case of Acquired Hemophilia B in a Patient with HIV Infection: Case Report and Literature Review.

Acquired hemophilia B is a rare bleeding disorder in which circulating specific antibodies inhibit the coagulation factors. Usually, it is associated with autoimmune diseases, malignancy and some infections such as hepatitis B (HBV) and C (HCV) viruses. The association with the human immunodeficiency virus (HIV) is rare. We present the first case of hemophilia B acquired in a patient with HIV. A 36-year-old woman with a history of HIV infection stage 3 acquired immunodeficiency syndrome (AIDS) (CDC 2014) and glomerulopathy secondary to HIV. She consulted for subacute non-dysenteric diarrhea. During her hospitalization, bacteremia by methicillin-sensitive Staphylococcus aureus (S.aureus) was documented, requiring hemodialysis catheter replacement with profuse bleeding during the procedure. The coagulation tests showed prolonged activated partial thromboplastin time (aPTT), normal prothrombin time (PT), mixing test with Rosner index: 8.8%, negative lupus anticoagulant, and specific tests for normal factor VIII and XI. The activity of factor IX was <50% and the inhibitor was increased, which confirms the diagnosis of hemophilia B. Acquired hemophilia B in a patient with HIV infection is not a frequent association; it should be suspected in the context of bleeding with prolonged aPTT.

A 52-Year-Old Man With Chest Pain and Dyspnea.

A 52-year-old man came to the cardiac surgery clinic for pulmonary thromboendarterectomy (PTE) evaluation. He had initially appeared at an outside hospital 1 year earlier, with chest pain and shortness of breath. He had no known chronic conditions. A CT pulmonary angiogram (CTPA) at that time showed a filling defect at the bifurcation of the main pulmonary artery. A transthoracic echocardiogram revealed mild mitral valve regurgitation, but otherwise the results were normal. As he was hemodynamically stable and not hypoxemic, he was treated solely by anticoagulation. Despite adhering to prescribed apixaban, he developed progressive dyspnea and reduced exercise tolerance over the subsequent year. A repeat CTPA performed 12 months after the initial presentation showed a persistent filling defect at the level of the pulmonary artery bifurcation, with a new extension now completely occluding the right main pulmonary artery. A pulmonary angiogram confirmed this complete occlusion, and right heart catheterization revealed precapillary pulmonary hypertension, with a mean pulmonary artery pressure of 50 mm Hg. His anticoagulation was transitioned to enoxaparin for presumed apixaban treatment failure, and an investigation for hypercoagulable conditions was initiated. His lupus anticoagulant test result was positive, but he did not meet the criteria for antiphospholipid syndrome because he was negative for anticardiolipin and β<sub2</sub-glycoprotein antibodies. Assays for antithrombin III, protein C, prothrombin gene, and factor V Leiden mutations produced normal results.

PCO2

Medicine In medicine, the partial pressure of carbon dioxide in arterial blood is called or PaCO2. Measurement of in the systemic circulation indicates the effectiveness of ventilation at the lungs' alveoli, given the diffusing capacity of the gas. It is a good indicator of respiratory function and the closely related factor of acid–base homeostasis, reflecting the amount of acid in the blood (without lactic acid). Normal values for humans are in the range 35–45 mmHg. Values less than this may indicate hyperventilation and (if blood pH is greater than 7.45) respiratory alkalosis. Values greater than 45 mmHg may indicate hypoventilation, and (if blood pH is less than 7.35) respiratory acidosis. Aquatic Sciences

The clinical spectrum of acute renal infarction.

Acute renal infarction is an oft-missed diagnosis. As a result, its true incidence, although presumed to be low, is actually unknown. Surprisingly, the medical literature on the subject, other than anecdotal case reports, is scarce. To increase physician awareness of the diagnosis and to identify predictive clinical and laboratory features of the entity. Between 1 November 1997 and 31 October 2000, 11 cases of acute renal infarction in 10 patients were diagnosed in our center by contrast-enhanced computerized tomography. The medical charts of these patients were reviewed regarding risk factors, clinical presentation, possible predictive laboratory examinations, and outcome. During the 36 month observation period, the incidence of acute renal infarction was 0.007%. The mean age of the patients (5 men and 5 women) was 67.4 +/- 21.1 (range 30-87 years). In four cases the right and in five the left kidney was involved; in the other two cases bilateral involvement was seen. In 7/10 patients, an increased risk for thromboembolic events was found. Six had chronic atrial fibrillation and one had a combined activated protein C resistance and protein S deficiency. Three patients had suffered a previous thromboembolic event. Two cases were receiving anticoagulant therapy with an INR of 1.6 and 1.8, respectively. On admission, flank pain was recorded in 10/11, fever in 5 and nausea/vomiting in 4 cases. Hematuria was detected in urine reagent strips in all cases. Serum lactate dehydrogenase and white blood cell count were elevated in all cases (1,570 +/- 703 IU/L and 12,988 +/- 3,841/microliter, respectively). In no case was the diagnosis of acute renal infarction initially entertained. The working diagnoses were renal colic in 2, pyelonephritis in 3, renal carcinoma, digitalis intoxication, and suspected endocarditis in one patient each, and an acute abdomen in 3. Time from admission to definitive CT diagnosis ranged from 24 hours to 6 days. Three patients were treated with intravenous heparin and another with a combination of i.v. heparin and renal intra-arterial urokinase infusion with, in the latter case, no recovery of function of the affected kidney. With the exception of this one patient (with a contralateral contracted kidney) who required maintenance dialysis, in all other cases serum creatinine levels remained unchanged or reverted to the baseline mean of 1.1 mg/dl (0.9-1.2). Acute renal infarction is not as rare as previously assumed. The entity is often misdiagnosed. Unilateral flank pain in a patient with an increased risk for thromboembolism should raise the suspicion of renal infarction. In such a setting, hematuria, leucocytosis and an elevated LDH level are strongly supportive of the diagnosis.

Acquired hemophilia A presenting as progressive intra-abdominal hemorrhage, muscle hemorrhage and hemothorax postpartum: A case report and literature review.

Acquired hemophilia A (AHA) is a rare antibody-mediated condition in which autoantibodies form against a coagulation factor, most commonly factor VIII (FVIII), causing severe coagulopathy. Here the present report presents a case of AHA in a 35-year-old postpartum woman with continuous polyserous bloody effusions who was admitted to the First Affiliated Hospital of Zhejiang Chinese Medical University (Hangzhou, China) in October 2017 without a history of trauma, anticoagulation treatment or coagulopathy. At presentation, the patient's hemoglobin level was low (70 g/l; normal range: 115-150 g/l) g/l, blood pressure was 89/58 mmHg (normal range, 90-140/60-90 mmHg), and activated partial thromboplastin time was 68.4 sec (normal range: 25.0-36.0 sec), with a normal international normalized ratio (0.94; normal range, 0.8-1.2). The reaction time in thrombography was prolonged (35.8 min; normal range: 5-10 min), coagulation FVIII had markedly decreased activity (12.6%; normal range, 60-150%), and FVIII inhibitor had a high titer [7.4 Bethesda units (BU)/ml; normal range, 0-0.6 BU/ml]. Notably, the patient's autoantibody level was markedly higher than normal (1:320; normal range: <1:100). The patient was successfully treated with bleeding control, eradication of FVIII inhibitor, and treatment of the underlying disease. To the best of our knowledge, this is the first case of AHA with polyserous bloody effusions in a patient with an autoimmune disorder during the postpartum period. Reports of such rare cases will aid the characterization of disease pathogenesis, which may in turn lead to the recognition and timely treatment of this rare disorder.

[Chance finding of a bilateral central pulmonary embolism while using cardiac computed tomography for the clarification of a coronary anomaly].

A 42 year-old man reported transient breathlessness and chest pain on the first day after a four-hour flight. During the following five months the symptoms recurred four times. After another episode he went to an outpatient department for further assessment. Blood tests demonstrated slightly elevated LDH (343 U/l) and also a minor increase of the D-dimers (710 microg/l). Hypercholesterolemia was also found (LDL-cholesterol 180 mg/dl). The rest of the blood tests, including the cardiac enzymes, were within normal limits. The electrocardiogram (ECG) showed sinus rhythm, heart rate 85 bpm and pre-terminal T-negativity in the precordial leads V1 to V3. Resting echocardiography and chest X-ray showed no significant abnormalities. The exercise ECG demonstrated no further ECG changes. However, because of the symptoms and a cardiovascular risk profile (family history, hypercholesterolemia and smoking) a coronary angiography was performed, which excluded coronary artery disease but revealed a so-called "right-sided single coronary artery", the left and right coronary arteries originating with a common stem from the right sinus of valsalva. To define the exact course of the left main coronary artery (whether in front of the pulmonary artery, between the two great arteries, retroaortic or septal) a contrast-enhanced cardiac computed tomography (CT) was performed, which demonstrated an anomalous position of the left main coronary artery in front of the pulmonary artery. Bilateral pulmonary embolism was an additional and unexpected finding. Oral anticoagulation was initiated after a coagulopathy had been excluded. The ultrasonography of the leg did not demonstrate any thrombosis. There was no evidence of malignant disease. Mild symptoms and absence of right heart congestion do not exclude pulmonary embolism. Depending on the symptoms and history, pulmonary thrombembolism has to be considered, especially if cardiac or extra-cardiac causes have been eliminated. The diagnostic method of choice for the detection or exclusion of pulmonary embolism is contrast-enhanced multi-slice spiral CT.

[Five cases of disseminated intravascular coagulation after peritoneojugular shunt by Le Veen valve].

The authors report the cases of five cirrhotic patients who underwent peritoneo-venous bypass via a Le Veen valve. Coagulation studies revealed on the one hand a worsening in certain pre-existent abnormalities (thrombocytopaenia, decrease in plasma coagulation factor levels), and secondly a frank increase in F.B.P and positivation of the transfer test. Clinically, two haemmorrhagic syndromes were seen, one of which was fatal. At no time was euglobulin lysis time less than 30 minutes. The administration of small doses of heparin corrected these laboratory abnormalities in all patients and stopped haemorrhage in one. These findings as a whole indicate that in these five cases the bypassing of ascites fluid led to a state of disseminated intravascular coagulation.

Protein S deficiency

Mutations in this condition change amino acids, which in turn disrupts blood clotting. Functional protein S is lacking, which normally turns off clotting proteins, this increases risk of blood clots. Diagnosis The diagnosis for deficiency of protein S can be done via reviewing family history of condition and genetic testing, as well as the following: Protein S antigen test Coagulation test (prothrombin time test) Thrombotic disease investigation Factor V Leiden test Differential diagnosis Among the possibilities for differential diagnosis of protein S deficiency are- Antiphospholipid syndrome, disseminated intravascular coagulation and antithrombin deficiency (though this list is not exhaustive)


Dendritic corneal ulcer is typical of herpes simplex keratitis. It presents with pain, not too striking, and scarce or absent red eye. There are ulcers resembling dendrites that may confuse us in the diagnosis. These pseudodendrites are found in herpes Zoster and in corneal abrasions in resolution. Although in practice we should pay attention to the shape of the dendrite (the true dendrite is deeper and has terminal bulbs at the end of each branch), and pay attention to the evolution of the pain (in the pseudodendrite after abrasion the pain should improve), when answering a MIR question it is simpler: if it is a dendrite, the first thing we have to think is herpes. Fungal and bacterial keratitis have corneal infiltrates. And glaucomatocyclitic crisis (Posner Schlossman syndrome) is a type of idiopathic hypertensive anterior uveitis, which does not present with ulceration.

A 35-year-old man comes to the emergency department with pain in his right eye of 3 days' evolution. Biomicroscopic examination of the anterior segment shows, after fluorescein staining, a central corneal ulcer in the form of a dendrite. What is the diagnosis?

Keratitis caused by Verticillium species.

To report a case of fungal keratitis caused by Verticillium species. A 50-year-old man developed pain, redness, and an infiltrate in his left eye and had no history of trauma. The cornea showed superficial, white, stromal infiltrates and epithelial ulceration with a dendritic margin. The clinical features suggested herpetic keratitis, and the patient was treated with topical antiviral medication. Two weeks later, his condition deteriorated. Examination of the left eye showed stromal infiltrates with a feathery margin and epithelial ulceration with its covering white exudates. Corneal scrapings were taken for direct microscopic examination and culture. Corneal scraping showed the presence of fungal filaments. The fungus was identified as Verticillium species. Topical amphotericin B and systemic fluconazole were started after discontinuing the antiviral treatment. Clinically, the inflammation subsided during the 3 weeks after treatment. This is a rare case of infectious keratitis caused by Verticillium species. Rare species of fungal infection should be considered in the differential diagnosis of stromal keratitis refractive to conventional medical treatment.

Christmas eye

Diagnosis Before confirming the diagnosis, it's important to keep in mind that there are similar conditions that demonstrate similar signs and symptoms, such as herpes keratitis, corneal abrasion and infectious corneal ulcer. In order to diagnosis Christmas Eye, it’s essential to take a look at the history, meaning what the patient was doing prior to attending the emergency room or a day before. Also, particular attention should be placed on the timeline of the pain and discomfort. Biomicroscopy will show the extent of corneal damage and amount of remaining epithelium present, which will assist in providing a confirmation of the diagnosis.

New-onset herpes simplex virus keratitis after cataract surgery.

We report the case of a 34-year-old man who had uncomplicated cataract surgery in his left eye. Medical history was significant for atopic dermatitis, requiring oral immunosuppressive medications. Two days after the surgery, the patient presented with pain, photophobia, decreased vision, and a small corneal abrasion. On postoperative day 5, the patient returned with left upper lid vesicular lesions and 2 corneal dendrites. Corrected vision was 20/100 OS, with intraocular pressure of 18 mm Hg and 1+ pigmented cells in the anterior chamber. Cultures of the lid lesions revealed herpes simplex virus (HSV) type 1. The patient was placed on oral acyclovir 800 mg 5 times a day. By day 8, the dendrites had resolved, and by day 15, the lid lesions healed over. HSV keratitis is an uncommon complication after cataract surgery. Ophthalmologists should be aware of the possibility of developing HSV keratitis even after the most routine cataract extraction.

[Painless acanthamoeba keratitis].

Acanthamoeba keratitis is a severe, painful corneal infection found in contact lens wearers. The entity can easily be confused with herpetic or fungal keratitis, especially if no ocular pain is reported. A 32-year old myopic female presented a unilateral keratitis of unknown etiology since 3 weeks. Administration of topical antiviral substances and corticosteroids led only to temporary improvement of the condition. The patient complained of photophobia but not of ocular pain. The affected eye showed corneal edema, central stromal thickening, descemet's striae as well as fibrin deposits on the corneal endothelium and in the anterior chamber. An aqueous specimen was negative for a viral infection. A culture for bacteria was negative. Staphylococci were cultured from corneal scrapings and Enterococci from the contact lens solution. Another corneal scraping revealed Acanthamoeba class II (6 weeks after the onset of symptoms). Under treatment with propamidine, polymyxin b, neomycin, gramicidin and polyhexidine (topical) as well as fluconazole/ketoconazole (systemic) the diameter of the annular infiltrate, which had developed decreased, but the infiltrate persisted. In the further course, the infiltrate persisted while the amount of fibrin in the anterior chamber increased. Penetrating keratoplasty was performed. Histologic examination of the host corneal tissue revealed massive infiltration with Acanthamoeba. Severe pain and history of wearing contact lenses are features suggestive of Acanthamoeba keratitis. The patient presented here had a history of contact lens wear, but no ocular pain was reported. The characteristic annular infiltrate had a late onset. Bacterial superinfection could not be ruled out. Therapeutic penetrating keratoplasty had to be performed as the condition deteriorated inspite of intensive chemotherapy. With penetrating keratoplasty a good visual acuity could be regained.

[Delayed course of Acanthamoeba keratitis].

A 35-year-old male presented with corneal ulceration on the left eye with a history of treatment over several months. At the first visit in our department we saw an elliptically shaped ulcerative stromal keratitis with circular peripheral neovascularization. There was organized hypopyon with hyphemia. The best corrected visual acuity (BCVA) was light perception. The patient had used contact lenses for many years. Under the suspicion of herpetic keratitis due to a positive "dendrite" the patient had undergone antiviral therapy for 6 months in a different department. Our diagnosis was Acanthamoeba keratitis. We performed penetrating excimer laser keratoplasty-à-chaud (8.0 × 7.0 mm/8.1 × 7.1 mm) with simultaneous cryotherapy of the mid-peripheral cornea. The topical therapy was polyhexamethylene biguanide, propamidine isoethionate, neomycin and steroids in intervals. A repeat penetrating excimer laser keratoplasty (8.5 × 7.5 mm/8.6 × 7.6 mm) with simultaneous amniotic membrane patch and lateral tarsorrhaphy was performed 2 months later due to melting of the graft with positive Seidel test. After successful surgery of the mature cataract the BCVA was 20/25. In a patient with a positive contact lens history acanthamoeba keratitis should always be considered as a differential diagnosis to herpes simplex keratitis in the early course of the disease.

Herpes zoster ophthalmicus

Epithelial: punctate epithelial erosions and pseudodendrites: often have anterior stromal infiltrates. Onset 2 to 3 days after the onset of the rash, resolving within 2–3 weeks. Common. Stromal: Nummular keratitis: have anterior stromal granular deposits. Occurs within 10 days of onset of rash. Uncommon Necrotising interstitial keratitis: Characterised by stromal infiltrates, corneal thinning and possibly perforation. Occurs between 3 months and several years after the onset of rash. Rare. Disciform Keratitis (Disciform Endotheliitis): a disc of corneal oedema, folds in Descemet's membrane, mild inflammation evident within the anterior chamber and fine keratic precipitates. Chronic. Occurs between 3 months and several years after the onset of the rash. Uncommon. Neurotrophic: corneal nerve damage causes a persistent epithelial defect, thinning and even perforation. The cornea becomes susceptible to bacterial and fungal keratitis. Chronic. Late onset. Uncommon.

Herpes simplex keratitis

Recurrent eye infection Recurrent herpes of the eye is caused by reactivation of the virus in a latently infected sensory ganglion, transport of the virus down the nerve axon to sensory nerve endings, and subsequent infection of ocular surface. The following classification of herpes simplex keratitis is important for understanding this disease: Dendritic ulcer (Epithelial keratitis) This classic herpetic lesion consists of a linear branching corneal ulcer (dendritic ulcer). During eye exam the defect is examined after staining with fluorescein dye. The underlying cornea has minimal inflammation. Patients with epithelial keratitis complain of foreign-body sensation, light sensitivity, redness and blurred vision. Focal or diffuse reduction in corneal sensation develops following recurrent epithelial keratitis. In immune deficient patients or with the use of corticosteroids the ulcer may become large and in these cases it is called geographic ulcer.

A Case of Herpetic Keratitis in an Orthokeratology Contact Lens Wearer.

We report a case of herpetic keratitis in an orthokeratology lens wearer. A 17-year-old man who wore an overnight orthokeratology lens for correction of myopia presented to our hospital with pain, lacrimation, and blurred vision affecting the left eye. His corrected visual acuity decreased to 18/20, and he showed dendrites and decreased corneal sensitivity in the left eye. The herpes simplex virus (HSV) immunochromatographic assay kit for the diagnosis of herpes epithelial keratitis was positive. As these findings were suggestive of HSV keratitis, topical acyclovir ointment was administered five times daily. All findings disappeared and visual acuity recovered to 20/20 at 14 days after the first visit. Herpetic keratitis rarely develops in orthokeratology lens wearers as well as contact lens (CL) wearers, although <iAcanthamoeba</i keratitis is sometimes erroneously diagnosed as herpetic keratitis in CL wearers with dendrites.

Acanthamoeba keratitis

Diagnosis Due to the relative rarity of Acanthamoeba keratitis (AK) compared to other causes of keratitis (bacterial, viral, etc.), it is often misdiagnosed, especially in the early stages of the disease. AK should be considered in all patients who use contact lenses, and following corneal abrasions or trauma. A thorough history should be obtained, especially relating to contact lens use and any recent changes contact in lens solution, exposure of the eyes to water or foreign objects, and symptoms that the patient is experiencing. The symptoms classically attributed to AK include decreased or blurred vision, sensitivity to light (photophobia), redness of the eye (conjunctival hyperemia), and pain out of proportion to physical exam findings. Another clinical feature that can distinguish Acanthamoeba from bacterial causes of keratitis is a lack of discharge from the eye.

Fungal keratitis

Pathophysiology The precipitating event for fungal keratitis is trauma with a vegetable / organic matter. A thorn injury, or in agriculture workers, trauma with a wheat plant while cutting the harvest is typical. This implants the fungus directly in the cornea. The fungus grows slowly in the cornea and proliferates to involve the anterior and posterior stromal layers. The fungus can break through the descemet's membrane and pass into the anterior chamber. The patient presents a few days or weeks later with fungal keratitis. Diagnosis The diagnosis is made by an ophthalmologist/optometrist correlating typical history, symptoms and signs. Many times it may be missed and misdiagnosed as bacterial ulcer. A definitive diagnosis is established only after a positive culture report (lactophenol cotton blue, calcoflour medium), typically taking a week, from the corneal scraping. Recent advances have been made in PCR ref 3./immunologic tests which can give a much quicker result.

Corneal ulcer

Many micro-organisms cause infective corneal ulcer. Among them are bacteria, fungi, viruses, protozoa, and chlamydia: Bacterial keratitis is caused by Staphylococcus aureus, Streptococcus viridans, Escherichia coli, Enterococci, Pseudomonas, Nocardia, N. Gonorrhoea and many other bacteria. Fungal keratitis causes deep and severe corneal ulcer. It is caused by Aspergillus sp., Fusarium sp., Candida sp., as also Rhizopus, Mucor, and other fungi. The typical feature of fungal keratitis is slow onset and gradual progression, where signs are much more than the symptoms. Small satellite lesions around the ulcer are a common feature of fungal keratitis and hypopyon is usually seen. Viral keratitis causes corneal ulceration. It is caused most commonly by Herpes simplex, Herpes zoster and Adenoviruses. Also it can be caused by coronaviruses & many other viruses. Herpes virus cause a dendritic ulcer, which can recur and relapse over the lifetime of an individual.

Epipremnum aureum Keratopathy: Case Report and Review of the Literature.

To report a novel case of Epipremnum aureum toxicity masquerading as bilateral infectious keratitis and review the literature on ocular manifestations of Epipremnum exposure. Case report and literature review. A 70-year-old man with a history of photorefractive keratectomy presented with a 3-day history of bilateral eye pain. The patient reported exposure to plant debris while performing yard work and also water exposure while cleaning his coral fish tanks. Clinical examination revealed bilateral epitheliopathy progressing to frank epithelial defects with underlying stromal necrosis 6 days after exposure. Empiric topical antibiotic drops were initiated, but multiple cultures, corneal biopsy, and confocal microscopy were all negative for an infectious agent. Over a 2-week period, the epithelial defects worsened and a suspicion for a toxic etiology was raised. The patient later recalled rubbing his eyes after exposure to Epipremnum aureum (Golden Pothos/Devils Ivy) sap. He was thus treated conservatively with artificial tears, topical corticosteroids, and amniotic membrane. After 3 months, the epithelial defects resolved, but with corneal scarring, prominently in the left eye and underwent penetrating keratoplasty. Five years after presentation, best-corrected visual acuity with hard contact lenses was 20/25 in the right eye and 20/20 in the left eye. Epipremnum aureum toxicity is a rare cause of keratitis. It can mimic acanthamoeba keratitis or anesthetic abuse and should be considered in cases of culture negative nonhealing corneal ulcerations. Eliciting a history of plant sap exposure can facilitate appropriate supportive care for this toxic keratitis.

Herpes simplex keratitis

Herpetic simplex keratitis is a form of keratitis caused by recurrent herpes simplex virus (HSV) infection in the cornea. It begins with infection of epithelial cells on the surface of the eye and retrograde infection of nerves serving the cornea. Primary infection typically presents as swelling of the conjunctiva and eyelids (blepharoconjunctivitis), accompanied by small white itchy lesions on the corneal surface. The effect of the lesions varies, from minor damage to the epithelium (superficial punctate keratitis), to more serious consequences such as the formation of dendritic ulcers. Infection is unilateral, affecting one eye at a time. Additional symptoms include dull pain deep inside the eye, mild to acute dryness, and sinusitis. Most primary infections resolve spontaneously in a few weeks. Healing can be aided by the use of oral and topical antivirals.

Fungal keratitis

Fungal keratitis is a fungal infection of the cornea, which can lead to blindness. It generally presents with a red, painful eye and blurred vision. There is also increased sensitivity to light, and excessive tears or discharge. It is caused by fungal organisms such as Fusarium, Aspergillus or Candida. Fungal keratitis has a worldwide distribution, but is more common in the tropics. Around 1 million people become blind every year due to fungal keratitis. Theodor Leber first described a case of fungal keratitis caused by Aspergillus in 1879. Signs and symptoms The symptoms of fungal keratitis typically emerge over 5-10 days and present with a painful eye, blurred vision, and redness of eye. There is increased sensitivity to light, and excessive tears or discharge. The symptoms are markedly less as compared to a similar bacterial ulcer. Symptoms may be noted to persist after contact lenses are removed, or following antibiotic treatment.

Herpes simplex keratitis

In immune deficient patients or with the use of corticosteroids the ulcer may become large and in these cases it is called geographic ulcer. Disciform keratitis (Endothelial keratitis) Endothelial keratitis manifests a central endothelitis in a disc-shaped manner. Longstanding corneal edema leads to permanent scarring and is the major cause of decreased vision associated with HSV. Localized endothelitis (localized inflammation of corneal endothelial layer) is the cause of disciform keratitis. Other forms Metaherpetic ulcer : is not due to live virus, results from inability of the corneal surface to heal. Necrotizing keratitis Keratouveitis : is usually granulomatous uveitis with large keratic precipitates on the corneal endothelium. Cause HSV is a double-stranded DNA virus that has icosahedral capsid. HSV-1 infections are found more commonly in the oral area and HSV-2 in the genital area. Ocular herpes simplex is usually caused by HSV-1. Diagnosis

Fungal keratitis

Signs: The eyelids and adnexa involved shows edema and redness, conjunctiva is chemosed. Ulcer may be present. It is a dry looking corneal ulcer with satellite lesions in the surrounding cornea. Usually associated with fungal ulcer is hypopyon, which is mostly white fluffy in appearance. Rarely, it may extend to the posterior segment to cause endophthalmitis in later stages, leading to the destruction of the eye. (Note: Fungal endophthalmitis is extremely rare) Causes Fungal keratitis has been reported to be caused by more than 70 different fungi, of which Fusarium, Aspergillus and Candida are responsible for 95% of cases. A. flavus and A. fumigatus are the most common types of Aspergillus to cause fungal keratitis. F. Solani is the most common type of Fusarium and others include Curvularia and Acremonium. C. albicans, C. guilliermondii and C. parapsilosis are the main types of Candida to cause fungal keratitis.

Herpes Simplex Keratitis -- History and Physical -- Corneal Epithelial Disease (Dendritic/Geographical Keratitis)

A past history of epithelial dendrite or a geographical is not always present, and a differential diagnosis of acanthamoeba and fungal keratitis should always be kept in mind.

Fungal Keratitis -- Differential Diagnosis

Bacterial keratitis Acanthamoeba keratitis Necrotizing herpetic keratitis

Fungal keratitis

Prognosis The infection typically takes a long time to heal, since the fungus itself is slow growing. Corneal perforation can occur in patients with untreated or partially treated infectious keratitis and requires surgical intervention in the form of corneal transplantation. Epidemiology This disease is quite common in the tropics and with large agrarian population. India has a high number of cases with fungal keratitis, but poor reporting system prevents accurate data collection. Florida in US regularly reports cases of fungal keratitis, with Aspergillus and Fusarium spp. as the most common causes. According to the Global Action Fund for Fungal Infections, every year there are around 1 million cases of blindness due to fungal keratitis. History A case of fungal keratitis caused by Aspergillus was first described by Theodor Leber in 1879, in a 54 year old farmer who injured his eye.

Corneal abrasion

About 3 per 1,000 people are affected a year in the United States. Males are more often affected than females. The typical age group affected is those in their 20s and 30s. Complications can include bacterial keratitis, corneal ulcer, and iritis. Complications may occur in up to 8% of people. Signs and symptoms Signs and symptoms of corneal abrasion include pain, trouble with bright lights, a foreign-body sensation, excessive squinting, and reflex production of tears. Signs include epithelial defects and edema, and often redness of the eye. The vision may be blurred, both from any swelling of the cornea and from excess tears. Crusty buildup from excess tears may also be present. Complications Complications are the exception rather than the rule from simple corneal abrasions. It is important that any foreign body be identified and removed, especially if containing iron as rusting will occur.

Acanthamoeba Keratitis -- Differential Diagnosis

Unlike patients with uncomplicated bacterial or fungal keratitis, patients with AK tend to be younger and often experience a more extended duration of symptoms at the initial presentation. [60] However, AK has been observed to coexist frequently with bacterial and fungal keratitis. [61] Consequently, the degree to which patients’ demographic factors should be considered in formulating a differential diagnosis remains unclear. The differential diagnosis for AK includes the following: Contact lens-associated keratitis Conjunctivitis Dry eye HSK: presents with dendritic or geographic ulcers Recurrent corneal erosion Staphylococcal marginal keratitis Fungal keratitis: has thicker infiltrates and is typically monofocal Bacterial keratitis

Bacterial Keratitis -- Differential Diagnosis -- Non- infective

Peripheral Ulcerative keratitis Marginal keratitis Mooren’s Ulcer Toxic keratitis Sterile inflammatory corneal infiltrate

Herpes simplex keratitis

Subsequent recurrences may be more severe, with infected epithelial cells showing larger dendritic ulceration, and lesions forming white plaques. The epithelial layer is sloughed off as the dendritic ulcer grows, and mild inflammation (iritis) may occur in the underlying stroma of iris. Sensation loss occurs in lesional areas, producing generalised corneal anaesthesia with repeated recurrences. Recurrence can be accompanied by chronic dry eye, low grade intermittent conjunctivitis, or chronic unexplained sinusitis. Following persistent infection the concentration of viral DNA reaches a critical limit. Antibody responses against the viral antigen expression in the stroma can trigger a massive immune response in the eye. The response may result in the destruction of the corneal stroma, resulting in loss of vision due to opacification of the cornea. This is known as immune-mediated stromal keratitis.

List of MeSH codes (C11)

– eye hemorrhage – choroid hemorrhage – hyphema – retinal hemorrhage – vitreous hemorrhage – eye infections – corneal ulcer – eye infections, bacterial – conjunctivitis, bacterial – conjunctivitis, inclusion – ophthalmia neonatorum – trachoma – hordeolum – keratoconjunctivitis, infectious – tuberculosis, ocular – uveitis, suppurative – endophthalmitis – panophthalmitis – eye infections, fungal – uveitis, suppurative – endophthalmitis – panophthalmitis – eye infections, parasitic – acanthamoeba keratitis – onchocerciasis, ocular – toxoplasmosis, ocular – eye infections, viral – conjunctivitis, viral – conjunctivitis, acute hemorrhagic – cytomegalovirus retinitis – herpes zoster ophthalmicus – keratitis, herpetic – keratitis, dendritic – eye manifestations

Successful Medical Management of Presumptive Pythium insidiosum Keratitis.

To describe the previously unreported successful treatment of presumptive Pythium keratitis (PK) with medical therapy alone. A 42-year-old female homemaker presented to us with a 15-day history of pain and redness in the right eye after a trivial injury. Her vision was 20/80 at presentation. Slit-lamp biomicroscopy revealed a central, dense and dry-looking, grayish-white infiltrate reaching mid stroma. The infiltrate had feathery margins and was surrounded by multiple tentacle-like lesions and peripherally expanding pinhead-sized subepithelial lesions. The contralateral eye was essentially normal. Diagnostic corneal scraping on smears revealed broad, aseptate, hyaline filaments with ribbon-like folds; very characteristic of Pythium species. Confocal imaging revealed fungal filaments. Based on corroborative evidence, a diagnosis of presumptive PK was made. She was administered a combination therapy consisting of eye drop linezolid 0.2% 1 hourly, azithromycin 1% 2 hourly, atropine sulfate 1% thrice daily, and oral azithromycin 500 mg once daily for 3 days in a week. After initial worsening in the form of stromal expansion, regression of pinhead-sized lesions was seen with onset of scarring by as early as day 4 of intense medical therapy. The tentacle-like lesions did not worsen. On day 8, significant resolution was noted with scarring, and by the end of 2 weeks, the entire stromal lesion had scarred and complete resolution of expanding tentacles was observed in 3 weeks. Presumptive Pythium keratitis of the patient completely resolved with antibacterial treatment alone. It is pertinent for ophthalmologists to be aware of this new treatment regimen.

List of MeSH codes (C11)

– corneal diseases – corneal dystrophies, hereditary – Fuchs' endothelial dystrophy – corneal edema – corneal neovascularization – corneal opacity – arcus senilis – keratitis – acanthamoeba keratitis – corneal ulcer – keratitis, herpetic – keratitis, dendritic – keratoconjunctivitis – keratoconjunctivitis, infectious – keratoconjunctivitis sicca – keratoconus – trachoma – eye abnormalities – aniridia – WAGR syndrome – anophthalmos – blepharophimosis – coloboma – ectopia lentis – hydrophthalmos – microphthalmos – retinal dysplasia

[The clinical features and study on therapeutic effects of fungal keratitis].

To review the clinical features and therapeutic effects of fungal keratitis (FK). 110 cases (110 eyes) with the disease were divided into two types: hyphomycetic keratitis in 94 eyes and candida keratitis in 16 eyes. The clinical features and therapeutic effects of the two types were observed and compared. The hyphomycetic keratitis generally had a plant traumatic history. The border of corneal infiltration was not clear with feather edges, and had a tendency to penetrate into the deep stroma of cornea. There were endothelial plaques, hypopyon and bad therapeutic effects. The pathogenicity of cardida keratitis (CK) was related to the local long-term use of glucocorticoid, the fungus seldom expanded into the deep corneal layers and infiltrated into the inner eye. Its therapeutic effects were better. The border of CK was characterized with limitations, and was clear. The clinical features of the two types are different. The clinical features caused by different or the same pathogenic fungi show great variations. Early diagnoses, correct use of medicine and operation are the key points to increase the curative rate.

Pythium Keratitis -- Differential Diagnosis

Fungal keratitis Bacterial keratitis Atypical Mycobacterial keratitis Acanthamoeba keratitis Necrotizing viral keratitis

Corneal Ulcer -- Evaluation

The patient with HSV keratitis or corneal ulcer will usually present similarly to the patient with bacterial keratitis. They will often have foreign body sensation, photophobia, conjunctival injection, and blurred vision. Slit lamp exam will classically reveal dendritic lesions with fluorescein uptake. [5]

[Severe microbial keratitis: report of 100 cases].

To study predisposing factors, clinical aspects, and microbiological diagnosis in severe microbial keratitis, and to discuss the therapy and visual outcome. and methods: A prospective and retrospective study concerning patients presenting microbial keratitis hospitalized in department B of the Hedi Raies Ophthalmology Institute (Tunis, Tunisia), from August 1996 to November 2004. One hundred patients with microbial keratitis were hospitalized (45 females and 55 males; ranging in age from 11 to 87 years). The principal predisposing factors were ocular surface pathology (30%), ocular trauma (28%), prior ocular surgery (17%), and contact lens wear (8%). The corneal scraping culture was positive in 42% of cases, isolating Gram-positive bacteria (48.6%), Gram-negative bacteria (29.7%), and fungi (21.6%). The majority of our patients (93%) had broad-spectrum topical antibiotics with therapeutic success in 53.8% of cases. Systemic antifungal agents were indicated in 17 cases. Surgery was necessary in 25.8% of cases: therapeutic keratoplasty in five cases and deleted keratoplasty in nine cases. Final visual acuity was equal to or better than at admission in 81% of cases. Anatomic loss of the eye was observed in eight cases (evisceration, six cases; enucleation, two cases). microbial keratitis is a frequent and severe pathology that can lead to blindness. Only early and adapted management can improve the prognosis of severe microbial keratitis.

[Painless acanthamoeba keratitis].

A 37-year-old contact lens wearer was treated for herpes simplex keratitis. After an initial improvement the keratitis became much worse. An annular infiltrate gave rise to the suspicion of acanthamoeba keratitis even though the patient was not in pain. This diagnosis was confirmed by histological and microbiological examination of the corneal disc after keratoplasty. Acanthamoeba keratitis should be considered even in the absence of pain, especially when the patients are contact lens wearers.

Keratitis

Keratitis is a condition in which the eye's cornea, the clear dome on the front surface of the eye, becomes inflamed. The condition is often marked by moderate to intense pain and usually involves any of the following symptoms: pain, impaired eyesight, photophobia (light sensitivity), red eye and a 'gritty' sensation. Classification (by chronicity) Acute Acute epithelial keratitis Nummular keratitis Interstitial keratitis Disciform keratitis Chronic Neurotrophic keratitis Mucous plaque keratitis Classification (infective) Viral Herpes simplex keratitis (dendritic keratitis). Viral infection of the cornea is often caused by the herpes simplex virus (HSV) which frequently leaves what is called a 'dendritic ulcer'. Herpes zoster keratitis, associated with herpes zoster ophthalmicus, which is a form of shingles.