Rapid Responses to:
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Rapid Responses: Rapid Responses published:
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HELLP syndrome
- Dr. Cristina Verdaguer (29 June 2007)
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Interactive case report
- DAVID GWYNFOR SAMUEL (29 June 2007)
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I'm glad the patient is there.
- Robert Bernstein (30 June 2007)
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Endothelial disorder
- David Mowbray (1 July 2007)
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Possible suggestions would be-
- Prasanta Padhan (1 July 2007)
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TTP
- Catie Butchart (1 July 2007)
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Stabilise then investigate
- Alasdair I Moonie (1 July 2007)
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Antiphospholipid syndrome +/- SLE???
- Vijay Zawar (2 July 2007)
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Delay in starting the plasma exchange = treatment failure
- Hawraman Ramadan (2 July 2007)
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Systematic approach is necessary
- Rishu Tandon (2 July 2007)
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Hypertension is the key
- C M Morgan (2 July 2007)
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Author interjection
- Chris M Laing (3 July 2007)
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? secondary TTP (related to collagen vascular disease)
- Thein H Oo, MD, FRCP (3 July 2007)
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hellp
- w afzal (4 July 2007)
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???Scleroderma renal crisis
- a anon (4 July 2007)
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TTP/HUS
- Seema Chakravarti (4 July 2007)
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???Scleroderma renal crisis - Addendum to ? secondary TTP (related to collagen vascular disease)
- Thein H Oo, MD, FRCP (4 July 2007)
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Catastrophic antiphospholipid syndrome
- Ken K Hodson (4 July 2007)
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Interactive case report: SLE most likely diagnosis
- fergus j dignan (5 July 2007)
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Underlying connective tissue disorder
- Faisal Mohammad (8 July 2007)
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Dr. Cristina Verdaguer, nephrologist Private Hospital 11200
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Would investigation for recurrent miscarriage have been appropriate
given the patient's reproductive history, and if so, how?
2 What diagnoses might explain the patient's presentation and the
abnormalities found?
3 What could account for the patient's chest radiography results?
4 Outline how the patient should be investigated and managed during the
first 24 hours
Competing interests: None declared |
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DAVID GWYNFOR SAMUEL, 4TH YEAR MEDICAL STUDENT MERTHYR TYDFIL CF47
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The case struck me as being very similar to one on my Gynaeocology attachment. The first thing to cross my mind was that this patient is suffering from (HELLP) Haemolysis,Elevated Lliver enzymes Low Platelets / Eclampsia, explained by the elevated BP, lowered platelet count, elevated LDH, lowered RBC, evidence of haemolyis by the RBC fragmentation and elevated reticulocyte count and slighlty deranged liver enzymes. In the short term her seizures should be controlled with the use of Magnesium Sulphate and establishing good airway control and maintainance. Her blood pressure should also be brought under control using i.v. labetalol or i.v. hydralazine. An Abdminal Ultrasound should be carried out to assess the uterine cavity. The Chest X-Ray suggests pulmonary oedmea and could be a result of her renal failure and uraemic status, indicated by a gorssley elevated 22.4 and Creatinine. I also questioned if she may have an underlying infection/ sepsis with organ failure due to the elevated WCC. She was possibly in ARDS due to the oedema and had a metabolic acidosis (Elevated LDH). I believe with her past obstetric history and her "Raynaud's" history an auto-immune screen is warranted to identify underlying conditions, inlcuding Anti Phospholid syndrome. I would include Anticardiolipin (IgG) and Anti b2 glycoprotein plasma protein antibodies and Lupus anticoagulant. I would also consider ANA and Anti Scl 70Ab screening for SLE. Competing interests: None declared |
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Robert Bernstein, Rheumatologist Manchester Royal Infirmary
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1 A couple of early miscarriages at this age are no hill of beans and need not have been investigated. 2 The first diagnosis to consider is thrombotic thrombocytopenic purpura, TTP: I expect the purpura is on its way, and I'm impressed by the illness, fits, pulmonary oedema, fragmented red cells, high LDH and normal clotting. Was TTP the paramedics' diagnosis, because TTP needs urgent plasmapheresis, and this patient has got to the Hammersmith and landed on 'Go'? The second diagnosis to consider is antiphospholipid syndrome, APLS (also sometimes called Whose Syndrome?). The miscarriages seem to have been rather early for this diagnosis. To seek APLS we need more sophisticated coagulation tests such as the dilute Russell viper venom test and an urgent anticardiolipin test. The quite short aPTT result makes this diagnosis less likely than TTP, though I suspect it is less rare overall. Can't we forget HELLP so early in pregnancy and with the pregnancy over? 3 The CXR appearances are nonspecific: pulmonary oedema, infection, haemorrhage, shock lung. In TTP and APLS the lung vessels may contain microthrombi, and in APLS there may be complement activation as well. 4 Blood and urine cultures as bacterial toxins can trigger TTP, platelet count on citrated blood to exclude clumping in the EDTA bottle, further clotting tests, fluids, fresh blood, antibiotics, plasma exchange, anti-platelet therapy probably, and thoughts of heparin and hysterectomy (so just as well I'm a knifeless rheumatologist). Competing interests: None declared |
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David Mowbray, consultant obstetrician Hereford County Hospital
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1. Investigation for recurrent miscarriage would not have been appropriate. However investigation of her hypertension and Raynauds symptoms for example to rule out SLE would have been indicated and helped pre-pregnancy counselling. 2. Haemolytic uraemic syndrome (HUS) or thrombotic thrombocytopaenic purpura (TTP). 3. Endothelial injury leading to vascular permeability exacerbated by the renal failure and hypertension. 4.Renal impairment/fluid overload - dialysis and renal ultrasound to rule out renal or post renal structural disease. Intravenous labetolol to control blood pressure. HUS/TTP - plasmapheresis Convulsions - phenytoin, when stable CT/MRI to rule out intracerebral pathology (oedema, haemorrhage) Vaginal bleeding - transvaginal sonography and SERUM hCG as very high levels (as in molar pregnancy)can lead to negative urine hCG. Obviously all of the above to be conducted in close co-operation with intensivists in an intensive care unit. Competing interests: None declared |
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Prasanta Padhan, Post Doctoral Fellow,Clinical Immunology and Rheumatology CMC,Vellore,632004,TN,India
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1)Patient should have been investigated for Antiphospholipid antibody syndrome(APS) for recurrent miscarriage. 2)A hemolytic uremic syndrome/Catastrophic APS secondary to lupus would be more likely diagnosis 3)Chest X ray findings are due to acute renal failure with fluid overload 4)Appropriate investigations will be ANA,Lupus anticoagulant,Anticardiolipin antibody,dsDNA,anti- Sm,C3,C4,24hr urinary protein,anti-Ro and anti-La. Initial management would be plasmapheresis,control of blood pressure,diuretics.If no response to consider termination of pregnancy. Competing interests: None declared |
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Catie Butchart, SpR Geriatrics/General Medicine Aberdeen
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1. No, but I would now want to investigate the possibility of autoimmune conditions as a cause for her presentation - SLE, antiphospholipid etc 2. Most likely diagnosis seems to be TTP - fever, malaise, headaches, seizures, low platelets, fragmented red cells, raised bilirubin and very high LDH. Other possibilities are HUS, antiphospholipid syndrome, sepsis (could the previous miscarriages have led to retained products of conception, leading to sepsis?). 3. CXR findings -most likely ARDS. Could have fluid overload but less likely. 4. Investigations: CT/MRI Brain, US pelvis, Blood and Urine Cultures, Autoantibodies including ANCA, anticardiolipin, anti dsDNA, complement levels Management: Early involvement of ITU, discuss with haematology for their advice and opinion, plasma exchange, dialysis, cover possibility of sepsis with broad spectrum antibiotics, treat hypertension, anticonvulsants. Competing interests: None declared |
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Alasdair I Moonie, Renal registrar St James's University Hospital, Beckett Street, Leeds, LS9 7TF
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This is a case of accelerated hypertension with acute renal failure, hypertensive encephalopathy, microangiopathic haemolytic anaemia and pulmonary oedema. The latter may be due to salt and water overload, hypertensive cardiomyopathy, ARDS or possibly bilateral renal artery stenosis. Potential diagnoses include untreated hypertension (most likely) and primary renal disease such as fibromuscular dysplasia and glomerulonephritis. Raynaud's and suspected recurrent miscarriages raises the possibility of connective tissue disease, in particular lupus and antiphospholipid syndrome. Thyroid crisis is very unlikely in the absence of prior symptoms, severe tachycardia or hyperpyrexia. Initial resuscitation must ensure airway patency, adequate oxygenation and seizure control. She is likely to require intubation if seizures are not terminated by IV lorazepam or phenytoin. She should be transferred to ICU for invasive BP and CVP monitoring. Further therapy should include rapid BP control, aiming for diastolic of 100-105. In the setting of pulmonary oedema, hydralazine and a diuretic would be appropriate followed by ACE inhibitor. Beta blockers should be avoided given the risk of further cardiac decompensation. If she remains oliguric then continuous veno-venous haemofiltration should be commenced aiming for gentle fluid removal (net 50-100mls/hr). Empirical immunosuppression is not indicated. Additional urgent investigations should include CT brain (to rule out haemorrhage) and bloods looking for primary renal disease (autoantibodies, anti-neutrophil cytoplasmic antibodies, anti-glomerular basement membrane antibody, immunoglobulins and serum electrophoresis, creatinine kinase). A renal biopsy would not be appropriate at this stage (low platelets, hypertension) though she should have urgent renal (looking for obstruction) and pelvic ultrasound. Competing interests: None declared |
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Vijay Zawar, Consultant Dermatologist Nashik, India
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This is an interesting presentation. Unfortunately, I do not have access to the complete article. Hence, do not know what have been worked out so far. However, reading the short version of the article, it sounds like antiphospholipid syndrome should be considered. This may occur without any identifiable cause(primary) or may be secondary to infectious etiology or collagen disease(mainly SLE)or due to certain drugs. Therefore, it is imperative to investigate this patient for anti- cardiolipin antibodies in addition to the work up for collagen profile (ANA, ds-DNA,etc.) It would be interesting to know as to what she turns up finally. Dr. Vijay Zawar, MD; DNB; DVD
Competing interests: None declared |
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Hawraman Ramadan, SpR Neurology Pinderfiel General Hospital, Wakefield
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1) yes, investigating this patients cause(s) of acute presentation
will explain cause of her previous miscarriages
Need regular monitoring FBC, clotting, U+E, LFT, glucose and ABG. In addition to noncontrast CT (to rule out haemorrhage), lupus anticoagulant, antiphospholid/anticardiolipine, ANCA, GBM, ANA and dsDNA antibodies Competing interests: None declared |
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Rishu Tandon, SSHO, obs&gynae UHW, Cardiff CF14 3NU
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1. Yes she should be investigated for recurrent pregnancy loss given the fact she has had live children with previous pregnancy. The presentation of her directs towards an infective etiology.Bloods should be taken for IgM& IgG 6 weeks apart , along with aCL antibodies, LAC.However they dont take priority while patient is in casuality struggling to be stabilised.TORCH screen can also be done although routinely it is not recommended for miscarriages . 2.Differential diagnosis 3. Chest X ray reveals patchy consolidation foci with evidence of pulmonary edema. consistent with ARDS. 4. Initial management includes hemodynamic stabilisation - CVP , crystalloids, broncodiators, iv steroids iv antibiotics including cover for aerobic and aanaerobic bacteria. As she convulsed , an urgent CT is indicated as a hemorrhagic stroke is a possibility . Appropriate monitoring of BP, urine output and inflammatory markers . Competing interests: None declared |
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C M Morgan, SHO O+G (GP VTS) Chesterfield Royal Hospital, S44 5BL
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1. Investigation for recurrent miscarriage would normally begin only after the third miscarriage, so prior to this event would not have necessarily been appropriate. 2. The most likely diagnosis would seem linked to her systemic hypertension. She has had previous pregnancy-induced hypertension, which would increase her risk of developing systemic hypertension later in life, and was noted to be hypertensive in the year preceding these events. Malignant or accelerated hypertension, resulting in malignant arteriolar nephrosclerosis with acute (?on chronic) renal failure and microangiopathic haemolytic anaemia (MAHA) would link all of the presenting features. Did she have papilloedema or hypertensive retinopathy out of interest? Differential diagnosis could include Thrombotic thrombocytopenic purpura (TTP) (but no purpura, and cannot link severe hypertension), systemic lupus erythematosus (SLE) with pre-existing renal involvement (but again I am struggling to link her gross hypertension with this as not classical), Pre-eclampsia/HELLP (but at 10 weeks it is probably too early for this), or sepsis, DIC and ARDS (but would more likely expect hypo- not hypertension). 3. The CXR can be explained by cardiac decompensation and bilateral pleural effusions. 4. She requires intensive monitoring with regular observation, most likely in a HDU/ITU setting, urinary catheterisation and strict fluid balance. A multi-disciplinary approach from cardiologists, nephrologists and intensive care specialists would be optimal. I would request a catheter spcimen urine for urgent microscopy (reducing the contamination from vaginal blood loss), perform an ECG, request a renal ultrasound and organise an autoimmune screen to complete investigations. The most important management step is reduction in blood pressure with careful monitoring as extreme sudden lowering of BP could result in infarction of vital organs. IV furosemide can be used to fluid offload and vasodilate. Hydralazine (iv or orally) and ACE inhibitors (to reduce high circulating renin levels) might be considered, as might a B-blocker such as labetalol, however given her pulmonary oedema, this might be best avoided. Competing interests: None declared |
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Chris M Laing, SpR nephrology and intensive care medicine Thames Region
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There have been some very interesting rapid responses here and the range of differential diagnoses suggested reflects the complexity of the case. Some of the responders have raised a number of very pertinent questions. Please be patient as these will be answered as the case unfolds over the next two parts. The differences of opinion on likely diagnosis have led to some disagreement on management, for example the appropriateness of the the use of plasma exchange and magnesium sulphate, though there is broad agreement on basic monitoring and stabilisation. I will not divulge whether the precise diagnosis has been mentioned in the responses, though this will become apparent. There is one important differential diagnosis that has not been mentioned that we at least considered on the basis of the information already presented. Inclusion of this differential would influence early management. Many thanks to the responders for their interest in this case. Competing interests: None declared |
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Thein H Oo, MD, FRCP, Attending Hematologist Caritas St Elizabeth's Medical Center, Tufts University School of Medicine, Boston, USA
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1. Investigation for recurrent miscarriage might have been appropriate. It'd be more interesting to know the timing of the previous miscarriages (i.e. within the first 8 weeks or early first trimester etc). This information will give us some hints whether miscarriage was due to chromosomal abnormalities versus placental vascular insufficiency . 2. The patient has (a) microangiopathic hemolytic anemia, (b) thrombocytopenia, (c) renal failure, (d) CNS changes such as headaches and convulsions. She also has past history of recurrent miscarriage, history suggestive of Raynaud's syndrome and hypertension. It'd have been worthwhile investigating the cause of hypertension 1 year ago. Could it be hypertension due to nephritis (with renal failure ) related to collagen vascular disease ? Is current renal failure acute-on-chronic renal failure ? Is thrombotic thrombocytopenic purpura primary versus secondary. If secondary, is it related to collagen vascular disease [1-4] ? 3. Chest radiograph also reveals pulmonary edema. 4. Having the above-mentioned thoughts in mind, I believe we should do the following; (a) admit the patient to intensive care unit. (b) management of airways, breathing per ICU team. (c) control of seizures. (d) control of hypertension. (e) several tubes and catheters - endotracheal tube and mechanical ventilation if necessary, nasogastric tube, indwelling foley catheters, IV access etc. (f) consult Hematology and Nephrology teams urgently. (g) Investigations - Blood - vonWillebrand's factor protease (ADAMTS- 13 enzyme ) activity, type & crossmatch, ANA, RF, ds-DNA, complement and vasculitic panels, etc, plasma protein immunofixation. Urine - urinalysis, urine for microscopy, 24-hour urine for protein, urine for immunofixation. (h)Place Vascath catheter. (i) This patient will need urgent therapeutic plasma exchange performed in tandem with hemodialysis (if feasible)[5]. The replacement fluid for plasmapheresis will be fresh frozen plasma. (j) systemic corticosteroids such as methylprednisone. (k) ICU management including strict intake-output data etc. (l) find out from GP if any investigations were done for miscarriage and hypertension and urgent review of the patient's old hospital chart. References: 1.Yamada T, Handa Y, Kamikawa T, et al. A case of systemic lupus erythematosus associated with thrombotic thrombocytopenic purpura and hemophagocytic syndrome].Nihon Rinsho Meneki Gakkai Kaishi 2006 Dec;29(6):384-8. Japanese 2.Majithia V, Harisdangkul V : Thrombotic thrombocytopenic purpura in systemic lupus erythematosus: A frequent and severe consequence of active disease. Rheumatology (Oxford). 2006 Sep;45(9):1170-1. 3.Cheung WY: Thrombotic thrombocytopenic purpura and systemic lupus erythematosus - distinct entities or overlapping syndromes? Transfus Apher Sci. 2006 Jun;34(3):263-6 4. Aleem A, Al-Sugair S. Thrombotic thrombocytopenic purpura associated with systemic lupus erythematosus. Acta Haematol. 2006;115(1-2):68-73 5. Mahmood A, Sodano D, Dash A, Weinstein R: Therapeutic plasma exchange performed in tandem with hemodialysis for patients with M-protein disorders. J Clin Apher 2006; 21(2):100-4 Competing interests: None declared |
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w afzal, gp reg de23 6ph
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This lady has the HELLP syndrome. The priority would be managing the seizures, pulmonary edema and maintaining the platelet count. Competing interests: None declared |
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a anon, . Aberdeen
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Just a long shot, but as you say there is one thing not yet mentioned, could it be ???scleroderma renal crisis sine sclerderma. I know it's very rare, but has been reported, and associated with pregnancy/miscarriage - Scand J Rheum 2003;32 (1):55-7. Should still treat as described in other responses - plasma exchange for ?TTP, dialysis, anticonvulsants, ITU admission etc.... Lower BP with ACE inhibitor ideally. Other investigations (in addition to those mentioned by others) should include anti-Scl-70 and anti-RNA polymerase III antibodies. Ideally would need renal biopsy, but likely too risky with low platelets and very high BP. Competing interests: None declared |
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Seema Chakravarti, Obstetric Consultant Queen's Hospital, Romford. RM7 0AG
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1 No if the previous pregnancy losses were less than 10 weeks gestation, then two miscarraiges would not be an indication for investigation. Also given her age she is more likely to miscarry anyway. If her pregnancies were complicated by pre-eclampsia (rather than non- proteinuric hypertension) and the babies were small for gestational age, then it may have been worth suggesting an APS screen. 2.TTP/HUS 3.ARDS 4.APS SCreen- acl/LA Double stranded DNA Complement levels vWillibrand cleaving factor Hourly urine output MRI Head Moniter pottasium levels BD liver/renal profile Plasmapharesis Consider dialysis dependin upon urine output Competing interests: None declared |
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Thein H Oo, MD, FRCP, Attending Hematologist Caritas St Elizabeth's Medical Center, Tufts University School of Medicine, Boston, USA
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Dear Dr Anon Thank you for raising this differential diagnosis. It's difficult to fit in how thrombocytopenia develops in this " scleroderma renal crisis." Unless, TTP develops in association with scleroderma in extremely rare circumstances ! That might have been the case. References: 1. Yusin J, Lewin K, Clements P. Thrombotic thrombocytopenia purpura in a patient with systemic sclerosis. J Clin Rheumatol. 2001 Apr;7(2):106-11 2. Manadan AM, Harris C, Block JA. Thrombotic thrombocytopenic purpura in the setting of systemic sclerosis. Semin Arthritis Rheum. 2005 Feb;34(4):683-8 3. Kfoury Baz EM, Mahfouz RA, Masri AF et al. Thrombotic thrombocytopenic purpura in a case of scleroderma renal crisis treated with twice-daily therapeutic plasma exchange. Ren Fail. 2001 Sep;23(5):737 -42 4. Towheed TE, Anastassiades TP, Ford SE et al. Thrombotic thrombocytopenic purpura as an initial presentation of limited systemic sclerosis. J Rheumatol. 1999 Jul;26(7):1613-6 Competing interests: None declared |
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Ken K Hodson, SpR Medicine (interest in Maternal Medicine) Royal Victoria Infirmary, Newcastle-upon-Tyne
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1. Investigation re: miscarriage - the patient is 46 yrs old and has had two previous successful pregnancies and two recent miscarriages from a new partner. Due to her age - the risk of miscarriage is much higher and given that she has had two previous pregnancies (albeit complicated by PET) whether to intensively investigate is difficult. Investigation would include screening for chromosomal (both her and partner) and autoimmune conditions such as SLE and antiphospholipid syndrome. Often screening is unproductive. 2. Diagnosis: TTP secondary to antiphospholipid syndrome. Patient has thrombocytopenia, renal failure, microcytic angiopathic haemolytic anaemia and neuro symptoms. Did she have fever? Malignant hypertension is a possibility (Raynaulds/hypertension - consider CREST as underlying cause for this). HELLP unlikely - as only early pregnant. Patient possibly has underlying vasculitis (note the raised BP a year earlier) 3. Pulmonary vascular leakage/ARDS. Differential would include causes of pulmonary-renal syndromes eg: Goodpastures, Wegner's Granulomatosis, Microscopic polyangiitis, Henoch- Schönlein purpura, IgA nephropathy, cryoglobulinemia, or pneumonia-related immune complex glomerulonephritis. 4. I would screen for vasculitis: ANA, RF, cANCA, pANCA, dsDNA, anti Rho, anti La, ENA lupus anticoagulant/anticardiolipin antibodies scl 70 and anticentromere antibodies (to exclude CREST) Cryoglobulins consider renal biopsy Needs supportive care: ITU, intubation/ventilation, dialysis if TTP - plasma exchange consider steroids/immunosuppression depending on results of vasculitis screen/exclusion of CREST. Competing interests: None declared |
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fergus j dignan, civilian medical practitioner RAF Lyneham SN15 4PZ
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1. I would not normally investigate the cause of 2 miscarriages in a woman in her 40's as the results would be unlikely to be helpful. 3 consecutive unexplained miscarriages, however, are more likely to have a common aetiology. 2. SLE is the most likely diagnosis as it fits the clinical picture and the blood results are all explainable by this disease. The CXR findings would be consistent with pulmonary oedema. This would be secondary to left ventricular failure secondary to hypertension secondary to chronic renal failure secondary to SLE. The convulsions were either caused by pre-eclampsia(a known complication of SLE in pregnancy) or hypocalcaemia, this in turn due to chronic renal disease. Thrombocytopaenia is a recognised feature of SLE, as is a haemolytic anaemia, as evidenced by the low Hb, high reticulocyte count, red cell fragmentation and very high LDH. 3. As already mentioned the CXR is consistent with pulmonary oedema. There is also probably left ventricular hypertrophy, accounted for by hypertension. 4. I would admit the patient to an ICU. Pre-eclampsia is likely to be the cause of the convulsions and these are likely to continue until the BP is brought down and for some time afterwards and so I would ventilate the patient. Having protected the airway my next priority is to get the BP down, using agents such as labetolol.Dexamethasone can be given for cerebral oedema (another reason for ventilation). The pulmonary oedema should respond to the hypotensive drugs but diuretics can also be administered. The hypocalcaemia should also be corrected. Blood should be taken for an auto immune profile with particular reference to anti ANA and anti DNA antibodies. Competing interests: None declared |
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Faisal Mohammad, SHO - Medical Rotation Arrowe Park Hospital Wirral NHS Trust,Arrowe Park Road,Wirral,CH49 5PE
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Some other responses have suggested HELLP syndrome, but patient had normal liver enzymes. I do not think that Eclampsia as a possible diagnosis as patient is not pregnant (negative HCG). 1)I would not investigate miscarriage at this point. 2)She has microangiopathic haemolytic anaemia and causes include HUS, TTP, Malignant hypertension and Vasculitis. Neurological involvement points towards TTP as well as Malignant Hypertension. In view of recurrent miscarriages and Raynauds I would consider underlying connective tissue disorder/Vasculitis on top of my differential diagnosis thus causing high blood pressure. Malignant hypertension can result in microangiopathic haemolytic anaemia, pulmonary oedema and renal failure. The underlying diagnosis could be SLE, Anti phospholipids syndrome or possible scleroderma with scleroderma crisis. 3)CXR showing pulmonary oedema is likely secondary to malignant hypertension. I would consider a fluid overload state in background of acute renal failure but there was no mention of ankle oedema or generalized swelling in the case report. 4)HDU / ITU admission BP needs to be controlled as it is the likely causes of seizures and requires gradual titration. Involve Haematology and Nephrology teams Autoantibody screen for above disorders and would consider plasmapharesis. Competing interests: None declared |
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