Get the usg done look for ureters & renal pelvis, occasionally while taking the angles during start and end of suturing the uterine incision, ureters are included. This happens specially when uterine incision is extended during delivery. I was entangled Once in such a situation i tied the lt ureter and latter done usg revealed congenital absence of rt kidney. We immediately opened her again and released the tie. That is why i always say to exteriorise the uterus to close its wound, this precaution wd keep the ureters away
Did you check patency of the urinary catheter.Sometimes if catheter is blocked there will not be any collection in the bag.
HELLP most likely cause d/d HUS / TTP / Hepatitis /ITP/ anti phospholipid syndrome/ lupus flare/AFLP We require the presence of all of the following criteria to diagnose HELLP (Tennessee classification) : ●Microangiopathic hemolytic anemia with characteristic schistocytes (also called helmet cells) on blood smear (picture 1). Other signs suggestive of hemolysis include an elevated indirect bilirubin level and a low serum haptoglobin concentration (≤25 mg/dL). ●Platelet count ≤100,000 cells/microL ●Total bilirubin ≥1.2 mg/dL (20.52 micromol/L) ●Serum AST >2 times upper limit of normal for local laboratory (usually >70 international units/L). Some investigators obtain alanine aminotransferase (ALT) levels instead of, or in addition to, AST levels. An advantage of the AST is that it is a single test that reflects both hepatocellular necrosis and red cell hemolysis. ●Severe renal insufficiency is suggestive of hemolytic uremic syndrome (HUS), which may be caused by a Shiga toxin-producing organism, complement regulatory defect (inherited or acquired), or drug. We do not treat HELLP syndrome with steroids. Initial observational studies and small randomized trials suggested use of glucocorticoids may be associated with more rapid improvement in laboratory and clinical parameters [37-40]. These findings were not supported by subsequent large, well-designed randomized, double-blind, placebo-controlled clinical trials evaluating the use of dexamethasone to improve maternal outcome in patients with HELLP syndrome Laboratory values may initially worsen following delivery. The time course of recovery from HELLP was evaluated in a series of 158 women with the disease . Decreasing platelet counts continued until 24 to 48 hours after delivery, while serum LDH concentration usually peaked 24 to 48 hours postpartum. In all patients who recovered, a platelet count greater than 100,000 cells/microL was achieved spontaneously by the sixth postpartum day or within 72 hours of the platelet nadir. An upward trend in platelet count and a downward trend in LDH concentration should be seen by the fourth postpartum day in the absence of complications. Others have reported similar findings . Recovery can be delayed in women with particularly severe disease, such as those with disseminated intravascular coagulation (DIC), platelet count less than 20,000 cells/microL, renal dysfunction, or ascites [19,64]. These women are at risk of developing pulmonary edema and renal failure.
The history may also suggest causes of prerenal AKI (such as hyperemesis gravidarum) or ATN/acute cortical necrosis (such as sepsis or hemorrhage related to obstetrical complications including placenta previa, prolonged intrauterine fetal death, or amniotic fluid embolism). All medications should be carefully reviewed. In addition to a careful history, physical examination, and medication review, we obtain the following tests: ●Dipstick urinalysis and microscopic analysis of sediment ●Quantitation of protein excretion by either 24-hour urine collection or by protein-to-creatinine ratio ●Urine culture ●Hemoglobin level and platelet count with peripheral blood smear to evaluate for microangiopathic hemolysis and thrombocytopenia ●Total, direct, and indirect bilirubin concentration; haptoglobin; and lactate dehydrogenase (LDH) to evaluate for hemolysis ●Serum aspartate aminotransferase (AST) and/or alanine aminotransferase (ALT) ●Renal ultrasound In addition to these tests, laboratory tests that suggest other, nonpregnancy-related causes of AKI may also be obtained (such as complement proteins C3, C4, antinuclear antibody [ANA], antineutrophil cytoplasmic antibody [ANCA], etc).
We electively initiate RRT prior to the development of severe electrolyte disturbances and volume overload. Thus, we favor electively initiating RRT in patients with K >5.8 to 6.0 mEq/L or severe metabolic acidosis (pH <7.2) despite optimal medical management and who show no sign that kidney function or metabolic acidosis is improving. We electively initiate RRT among patients who are repeatedly in positive fluid balance despite aggressive attempts at diuresis, particularly if they have increasing oxygen requirements. Observational studies have demonstrated an association between the severity of volume overload at the time of initiation of RRT and mortality risk [2-4]. In the absence of clinically significant uremic symptoms or specific indications such as severe electrolyte abnormalities or volume overload, the optimal timing of RRT initiation is controversial. We generally suggest not initiating RRT in the absence of these indications, particularly if the blood urea nitrogen (BUN) is <110 to 120 mg/dL.
Accepted urgent indications for RRT in patients with AKI generally include: ●Refractory fluid overload ●Hyperkalemia (plasma potassium concentration >6.5 mEq/L) or rapidly rising potassium levels ●Signs of uremia, such as pericarditis, encephalopathy, or an otherwise unexplained decline in mental status ●Severe metabolic acidosis (pH <7.1) ●Certain alcohol and drug intoxications
Drug treatments reported to be equivalent to clindamycin plus gentamicin include cefotetan, cefoxitin, ceftizoxime, piperacillin with or without tazobactam, and ampicillin and sulbactam [3,65-68]. These drugs, particularly ampicillin and sulbactam, are used as the initial antibiotic choice in some hospitals.
I.Check urinary catheter patency. 2.Do USG KUB 3.DO Electrolytes estimation.4.platlet r only 27,000/cmm so do coagulation profile. 5 look for haemorrhage concealed/revealed. 6 maintain input/output 7.Think of drug reaction leading to acute renal failure ? Cefalosporines.
The treatment of AKI is supportive. Dialysis should be initiated based on the usual criteria for patients in the nonobstetric setting and particularly if oliguria is present
The most common postpartum infection is endometritis. It is usually due to mixed flora, including anaerobic, gram negative, and gram positive organisms.
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HEMATOLOGICAL MANIFESTATIONS OF SLE SLE is the most common multisystem connective tissue disease characterized by *wide variety of clinical features. *presence of numerous auto-antibodies. *circulating immune complexes. *widespread immunologically determined tissue damage. Hematological manifestations include cellular elements of blood and coagulation pathway. The major hematological manifestations of SLE are 1.Anemia. 2.Leucopenia. 3.Thrombocytopenia. 4.Antiphospholipid syndrome. ANEMIA : Mechanisms which contribute to anemia are 1.Inflammation. 2.Renal insufficiency. 3.Blood loss. 4.Dietary insufficiency. 5.Medications. 6.Hemolysis. 7.Infection. 8.Hyperspleenism. 9.Myelodysplasia. 10.Aplastic anemia. 1.ANEMIA OF CHRONIC INFLAMMATION / CHRONIC DISEASE. Anemia of chronic inflammation is due to suppressed erythropoiesis.The type of anemia is *Normocytic,normochromic with a relatively low reticulocyte count. *Bone marrow iron stores are adequate. *Serum ferritin concentration elevated. In the absence of symptoms of anemia like dyspnea on exertion and easy fatiguability, anemia of chronic inflammation doesn't require treatment. Recombinant human erythropoietin or darbepoietin alfa can be used to stimulate erythropoesis. 2.ANEMIA OF RENAL INSUFFICIENCY: The cause of anemia is due to deficient production of erythropoietin by the diseased kidneys. INAPPROPRIATELY LOW LEVEL OF ERYTHROPOIETIN IS A HALLMARK OF ANEMIA OF RENAL INSUFFICIENCY. 3.ANEMIA OF BLOOD LOSS : Blood loss can be due to *Blood loss from GIT due to medications. NSAID's or steroids. *Menorrhagia. *Pulmonary hemorrhage. Symptoms of alveolar hemorrhage are dyspnea and cough.The presence of alveolar infiltrates on a chest radiograph or ground glass opacities on chest CT are suggestive of alveolar hemorrhage. 4.ANEMIA OF RED CELL APLASIA : Red cell aplasia can be caused by *Antibodies directed against erythropoietin. *Antibodies against bone marrow precursors. *Bone marrow suppression can be induced by medications like anti-malarial drugs and immunosupressants. This responds to immunosuppressive therapy. 5.AUTO IMMUNE HEMOLYTIC ANEMIA (AIHA) AIHA characterized by *elevated reticulocyte count. *low haptoglobulin levels. *increase indirect bilirubin concentration. *positive coombs' test. steroids,azathioprine,cyclophosphamide , spleenectomy ,intravenous immune globulin, danazol,mycophenolate mofetil and rituximab are various treatment modalities. 6.MICROANGIOPATHIC HEMOLYTIC ANEMIA Lupus is associated with thrombotic microangiopathic anemia manifested by a peripheral blood smear showing *schistocytes. *elevated levels of lactate dehydrogenase. *elevated levels of bilirubin. Severe MAHA (microangiopathic hemolytic anemia) is treated with plasmapheresis and plasma infusions. Less severe disease is treated with high dose corticosteroids.They are treated with plasmapheresis if they deteriorate or fail to improve with steroid treatment alone. Anemia of SLE is divided into *Impaired red cell production :marrow supression, nutrient deficiency. *Increased red cell destruction :hemolysis, hyperspleenism. *Blood loss. Measurement of reticulocyte production (RETICULOCYTE INDEX) is used to differentiate these anemias. IDA: Serum ferritin <<< 20 ug/dl. PERNICIOUS ANEMIA:Defined by *serum vitamin B12 <<<180 pmol/l. *abnormal schilling test. *presence of anti-intrinsic antibody in blood. Peripheral smears stained with wright's stain provides important clues to the diagnosis of anemias. *Spherocytes ,microspherocytes,elliptocytes indicate auto immune hemolytic anemia. *Fragmented RBC's :schistocytes,helmet cells indicate MAHA. *Acanthocytes :liver disease. *Blister /bite cells:oxidant-induced damage to the red cell &its membrane (G-6-PD ). *RBC with inclusions :malaria,babesiosis and bartonella infections. *Tear drop RBC's with circulating nucleated RBC and nucleated WBC forms :indicates the presence of marrow involvement ,as in primary myelofibrosis or tumour infiltration. *Increased reticulocyte count :hemolytic process or acute blood loss. *Inadequate reticulocytes :nutritional anemia of iron,vitamin B12 or folate. *Serum ferritin reduced :IDA. *Serum ferritin >>20ug/dl :anemia of chronic diseases. LEUCOPENIA ,NEUTROPENIA ,LYMPHOCYTOPENIA ,DECREASED EOSINOPHILS & BASOPHILS ,THROMBOCYTOPENIA ARE ALL SEEN IN SLE. To be continued for students.Dr. Suvarchala Pratap7 Likes10 Answers