Shattered. Third consecutive day of on-calls at the birth centre. I’m afraid I have little to show for it. The logbook hangs limply at my side, the pages where my name is printed await signatures; surrogate markers of new found skills. Half asleep I slump against the wall and cast my mind back to the peripheral attachment from which I have not long returned. The old-school consultant’s mutterings are still fresh: “Medical education was different back then you see....you are dealt a tough hand nowadays.” I quite agree, it is Saturday. Might it be said the clinical apprenticeship we know today is a shadow of its former self? Medical school was more a way of life, students lived in the hospital, they even had their laundry done for them. Incredulous, I could scarcely restrain a chuckle at the consultant’s stories of delivering babies while merely a student and how the dishing out of “character building” grillings by their seniors was de rigeur. Seldom am I plied with any such questions. Teaching is a rare commodity at times. Hours on a busy ward can bear little return. Frequently do I hear students barely a rotation into their clinical years, bemoan a woeful lack of attention. All recollection of the starry-eyed second year, romanced by anything remotely clinical, has evaporated like the morning dew. “Make way, make way!...” cries a thin voice from the far reaches of the centre. A squeal of bed wheels. The newly crowned obs & gynae reg drives past the midwife station executing an impressive Tokyo drift into the corridor where I stand. Through the theatre doors opposite me he vanishes. I follow. Major postpartum haemorrhage. A bevy of scrubs flit across the room in a live performance of the RCOG guidelines for obstetric haemorrhage. They resuscitate the women on the table, her clammy body flat across the carmine blotched sheets. ABC, intravenous access and a rapid two litres of Hartmann’s later, the bleeding can not be arrested by rubbing up contraction. Pharmacological measures: syntocinon and ergometrine preparations do not staunch the flow. Blood pressure still falling, I watch the consciousness slowly ebb from the woman’s eyes. Then in a tone of voice, seemingly beyond his years, the reversely gowned anaesthetist clocks my badge and says, “Fetch me the carboprost.” I could feel an exercise in futility sprout as I gave an empty but ingratiating nod. “It’s hemabate....in the fridge” he continues. In the anaesthetic room I find the fridge and rummage blindly through. Thirty seconds later having discovered nothing but my general inadequacy, I crawl back into theatre. I was as good as useless though to my surprise the anaesthetist disappeared and returned with a vial. Handing me both it and a prepped syringe, he instructs me to inject intramuscularly into the woman’s thigh. The most common cause of postpartum haemorrhage is uterine atony. Prostaglandin analogues like carboprost promote coordinated contractions of the body of the pregnant uterus. Constriction of the vessels by myometrial fibres within the uterine walls achieves postpartum haemostasis. This textbook definition does not quite echo my thoughts as I gingerly approach the operating table. Alarmingly I am unaware that aside from the usual side effects of the drug in my syringe; the nausea and vomiting, should the needle stray into a nearby vessel and its contents escape into the circulation, cardiovascular collapse might be the unfortunate result. Suddenly the anaesthetist’s dour expression as I inject now assumes some meaning. What a relief to see the woman’s vitals begin to stabilise. As we wheel her into the recovery bay, the anaesthetist unleashes an onslaught of questions. Keen to redeem some lost pride, I can to varying degrees, resurrect long buried preclinical knowledge: basic pharmacology, transfusion-related complications, the importance of fresh frozen plasma. Although, the final threat of drawing the clotting cascade from memory is a challenge too far. Before long I am already being demonstrated the techniques of regional analgesia, why you should always aspirate before injecting lidocaine and thrust headlong into managing the most common adverse effects of epidurals. To have thought I had been ready to retire home early on this Saturday morning had serendipity not played its part. A little persistence would have been just as effective. It’s the quality so easily overlooked in these apparently austere times of medical education. And not a single logbook signature gained. Oh the shame! This blog post is a reproduction of an article published in the Medical Student Newspaper, February 2014 issue.
over 5 years ago
Storylines on popular TV dramas are a great way of raising the public's awareness of a disease. They're almost as effective as a celebrity contracting an illness. For example, when Wiggles member Greg Page quit the group because of postural orthostatic tachycardia syndrome, I had a spate of patients, mostly young and female, coming in with self-diagnosed "Wiggles Disease". A 30% increase in the number of mammograms in the under-40s was attributed to Kylie Minogue's breast cancer diagnosis. The list goes on. Thanks to a storyline on the TV drama Desperate Housewives, I received questions about male postnatal depression from local housewives desperate for information: "Does it really exist?" "I thought postnatal depression was to do with hormones, so how can males get it?" "First it's male menopause, now it's male postnatal depression. Why can't they keep their grubby mitts off our conditions?" "It's like that politically correct crap about a 'couple' being pregnant. 'We' weren't pregnant, 'I' was. His contribution was five seconds of ecstasy and I was landed with nine months of morning sickness, tiredness, stretch marks and sore boobs!" One of my patients, a retired hospital matron now in her 90s, had quite a few words to say on the subject. "Male postnatal depression -- what rot! The women's liberation movement started insisting on equality and now the men are getting their revenge. You know, dear, it all began going downhill for women when they started letting fathers into the labour wards. How can a man look at his wife in the same way if he has seen a blood-and-muck-covered baby come out of her … you know? Men don't really want to be there. They just think they should -- it's a modern expectation. Poor things have no real choice." Before I had the chance to express my paucity of empathy she continued to pontificate. "Modern women just don't understand men. They are going about it the wrong way. Take young couples who live with each other out of wedlock and share all kind of intimacies. I'm not talking about sex; no, things more intimate than that, like bathroom activities, make-up removal, shaving, and so on." Her voice dropped to a horrified whisper. "And I'm told that some young women don't even shut the door when they're toileting. No wonder they can't get their de facto boyfriends to marry them. Foolish girls. Men need some mystery. Even when you're married, toileting should definitely be kept private." I have mixed feelings about male postnatal depression. I have no doubt that males can develop depression after the arrival of a newborn into the household; however, labelling it "postnatal depression" doesn't sit all that comfortably with me. I'm all for equality, but the simple fact of the matter is that males and females are biologically different, especially in the reproductive arena, and no amount of political correctness or male sharing-and-caring can alter that. Depressed fathers need to be identified, supported and treated, that goes without saying, but how about we leave the "postnatal" tag to the ladies? As one of my female patients said: "We are the ones who go through the 'natal'. When the boys start giving birth, then they can be prenatal, postnatal or any kind of natal they want!" (This blog post has been adapted from a column first published in Australian Doctor http://bit.ly/1aKdvMM)
Dr Genevieve Yates
almost 6 years ago
Based on presentation I gave as a medical student doing Obstetrics and Gynaecology in 2009. More details pertaining to each slide are in the Notes sections.
over 6 years ago
This month’s case is by David R Bell PhD, co-author of Medical Physiology: Principles for Clinical Medicine, 3e (ISBN: 9781451110395) For more information, or to purchase your copy, visit: http://tiny.cc/Rhoades4e, with 15% off using the discount code: MEDUCATION. The case below is followed by a quiz question, allowing you a choice of diagnoses. Select the one letter section that best describes the patient’s condition. The Case A 28-year old woman has an unremarkable pregnancy through her first 28 weeks of gestation, with normal weight gain and no serious complications. She has no previous history of diabetes, hypertension of other systemic disease before or during her current pregnancy. During her 30-week checkup, her blood pressure measures 128/85, and she complains about feeling slightly more “bloated” than usual with swelling in her legs that seems to get more uncomfortable as the day goes on. Her obsterician recommends that she get more bed rest, stay off her feet as much as possible and return for evaluation in one week. At the one-week follow-up, the patient presents with noticable”puffiness” in her face, and a blood pressure of 145/95. She complains she has been developing headaches, sporadic blurred vision, right-sided discomfort and some shortness of breath. She has gained more than 10 lb (4.5kg) in the past week. A urinalysis on the patient revelas no glucose but a 3+ reading for protein. Her obstetrician decides to admit her immediately to a local tertiary care hospital for further evaluation. Over the next 24 hours, the patient’s urine output is recorded as 500mL and contains 6.8 grams of protein. Her plasma albumin level is 3.1 g/dl, hemacrit 48%, indirect bilirubin 1.5mg/dl and blood platelets=77000/uL, respectively. Her blood pressure is now 190/100. It is decided to try to deliver the foetus. The expelled placenta is small and shows signs of widespread ischmic damage. Within a week of delivery, the mother’s blood pressure returns to normal, and her oedema subsides. One month later, the mother shows no ill effects of thos later-term syndrome. Question What is the clinical diagnosis of this patient’s condition and its underlying pathophysiology? A. Gestational Hypertension B. Preeclampsia C. Gestational Diabetes D. Compression of the Inferior Vena Cava Answer The correct answer is "B. Preeclampsia". The patient’s symptoms and laboratory findings are consistent with a diagnosis of Preeclampsia, which is a condition occurring in some pregnancies that causes life-threatening organ and whole body regulatory malfunctions. The patient’s negative urine glucose is inconsistent with gestational diabetes. Gestational hypertension or vena caval compression cannot explain all of the patient findings. The patient has three major abnormal findings- generalised oedema, hypertension and proteinuria which are all common in preeclampsia. Although sequalae of a normal pregnancy can include water and salt retention, bloating, modest hypertension and leg swelling (secondary to capillary fluid loss from increased lower limb capillary hydrostatic pressure due to compression of the inferior vena cava by the growing foetus/uterus), oedema in the head and upper extremities, a rapid 10 pound weight gain and shortness of breath suggests a generalized and serious oedematous state. The patient did not have hypertension before or within 20 weeks gestation (primary hypertension) and did not develop hypertension after the 20th week of pregnancy with no other abnormal findings (gestational hypertension). Hypertension with proteinuria occurring beyond the 20th week of pregnancy however is a hallmark of preeclampsia. In addition, the patient has hemolysis (elevated bilirubin and LDH levels), elevated liver enzyme levels and thrombocytopenia. This is called the HELLP syndrome (HELLP = Hemolysis, Elevated Liver enzymes and Low Platelets.), and is considered evidence of serious patient deterioration in preeclampsia. A urine output of 500 ml in 24 hours is 1/2 to 1/4 of normal output in a hydrated female and indicates renal insufficiency. Protein should never be found in the urine and indicates loss of capillaries integrity in glomeruli which normally are not permeable to proteins. The patient has substantial 24 urine protein loss and hypoalbuminemia. However, generally plasma albumin levels must drop below 2.5 gm/dl to decrease plasma oncotic pressure enough to cause general oedema. The patient’s total urinary protein loss was insufficient in this regard. Capillary hyperpermeability occurs with preeclampsia and, along with hypertension, could facilitate capillary water efflux and generalized oedema. However myogenic constriction of pre-capillary arterioles could reduce the effect of high blood pressure on capillary water efflux. An early increase in hematocrit in this patient suggests hemoconcentration which could be caused by capillary fluid loss but the patient’s value of 48 is unremarkable and of little diagnostic value because increased hematocrit occurs in both preeclampsia and normal pregnancy. PGI2, PGE2 and NO, produced during normal pregnancy, cause vasorelaxation and luminal expansion of uterine arteries, which supports placental blood flow and development. Current theory suggests that over production of endothelin, thromboxane and oxygen radicals in preeclampsia antagonize vasorelaxation while stimulating platelet aggregation, microthrombi formation and endothelial destruction. These could cause oedema, hypertension, renal/hepatic deterioration and placental ischemia with release of vasotoxic factors. The patient’s right-sided pain is consistent with liver pathology (secondary to hepatic DIC or oedematous distention). Severe hypertension in preeclampsia can lead to maternal end organ damage, stroke, and death. Oedematous distension of the liver can cause hepatic rupture and internal hemorrhagic shock. Having this patient carry the baby to term markedly risks the life of the mother and is not considered current acceptable clinical practice. Delivery of the foetus and termination of the pregnancy is the only certain way to end preeclampsia. Read more This case is by David R Bell PhD, co-author of Medical Physiology: Principles for Clinical Medicine, 3e (ISBN: 9781451110395) For more information, or to purchase your copy, visit: http://tiny.cc/Rhoades4e. Save 15% (and get free P&P) on this, and a whole host of other LWW titles at (lww.co.uk)[http://lww.co.uk] when you use the code MEDUCATION when you check out! About LWW/ Wolters Kluwer Health Lippincott Williams and Wilkins (LWW) is a leading publisher of high-quality content for students and practitioners in medical and related fields. Their text and review products, eBooks, mobile apps and online solutions support students, educators, and instiutions throughout the professional’s career. LWW are proud to partner with Meducation.
Lippincott Williams & Wilkins
over 6 years ago
Looking back on this past fortnight, I feel my tutor has been determined to engage me in absolutely everything, and I think it's worked. Whilst not a full blown ob/gyn enthusiast, I have to say I was surprised to admit today that I am enjoying myself. This leads me on to what this reflection is actually on. The preconceptions we hold about what we do, the people we see and the impact it has on us. What I will write about, I am writing about partly because I have had instances where this has happened recently and I have felt fairly guilty, and partly because I want to know if this happens to everyone else (or if I'm just one insensitive individual!!) Now this isn't going to be a very long draft of wisdom that will be quoted by people when I'm long gone, mainly because the phrase 'never judge a book by it's cover,' has been around for god knows how long, but I do feel it's surprising the extent to which I had dismissed that saying, which I had only just realised today. I am fairly certain, that whilst it's not talked about much, most people decide how they're going to speak to other people (keep in mind this is mostly going to be a subconscious process) and act around them when they see them and interact. I am also fairly certain that doctors do this with patients and that this isn't probably innocent and maybe it does impact on the delivery of care. You see a person with bedraggled hair, poor dental hygiene, clothes that look like they haven't been washed, for example, and all the associations that come with that flood into your brain, whether they are false or accurate. Or an individual with an Omega watch, designer clothing with everything in pristine condition. I am willing to bet those two descriptions conjured completely different images of person in your head. More than just the physical image though, there were different lifestyles and choices in life. And would they get different approaches? Maybe. I'm not sure if we are able to switch off the instant preconceptions, but we have to hide them as whilst they may be accurate, there's an equal chance they may be inaccurate! I can tell it's certainly difficult sometimes, yet people manage in the name of professionalism. I think I'm rambling, so I'll end this piece with this: I just wonder if people can tell what you think about them. In an environment where you have to treat everyone equally and preconceptions must be overcome, can the patients see some reaction in the faces of staff that translates for a split second everything that pops into the mind? There may well be a social study on it somewhere, I may look if I get time and if I find one I shall post it. I'd be interested to hear others experiences or thoughts on this topic too!
over 6 years ago
In the case of severe postpartum haemorrhage, is it always necessary to give packed red cells?
almost 8 years ago
Topics This morning, I’m talking about Bartholin cysts. Bartholin Cyst and Abscess… View Text Here Draining a Bartholin Cyst Video… View Free Video Here Commercial Links: 5-Minute Bartholin Cyst Vide 5-Minute Vulvar Biops 5-Minute Vulva Anatomy Video Free Links: OBGYN-10 OBGYN-101 Gray Haired Note Simple Operations of the Vulva in the Global Library of Women’s Medicin Brookside Associates Medical Education Division
Mike Hughey, MD
about 9 years ago
Topics This afternoon, I’d like to talk about an important complication of delivery, called shoulder dystocia. Shoulder Dystocia… View Text Here Delivery of the Posterior Arm Video… View Free Video Here Commercial Links: Shoulder Dystocia Vide 5-Minute Vaginal Delivery Vide 5-Minute Episiotomy Video Free Links: OBGYN-10 OBGYN-101 Gray Haired Note Shoulder Dystocia in the Global Library of Women’s Medicin Brookside Associates Medical Education Division
Mike Hughey, MD
about 9 years ago
Topics Today I’ll discuss the clinical management of abnormal Pap smears that do not involve obvious dysplasia or cancer of the cervix. Pap Smear Interpretation and Management of Abnormals… View Text Here Pap Smear Video… View Free Video Here Commercial Links: Dysplasia Vide Colposcopy Vide 5-Minute Pap Smear Video Free Links: OBGYN-10 OBGYN-101 Gray Haired Note Cervical Intraepithelial Neoplasia: History and Detection, in [...]
Mike Hughey, MD
about 9 years ago
Topics This afternoon, I’l be discussing the obstetrical problems of pre-eclampsia and eclampsia. Hypertensive Issues During Pregnancy… View Text Here Free Links: OBGYN-10 OBGYN-101 Gray Haired Note Pre-eclampsia and Eclampsia, in the Global Library of Women’s Medicin Chronic Hypertension in Pregnancy, in the Global Library of Women’s Medicin Brookside Associates Medical Education Division
Mike Hughey, MD
about 9 years ago
Topics Today, I’ll discuss the inherent contraction patterns of the uterus as they vary throughout the menstrual cycle and the role that may play in sperm transport, infertility, endometriosis and contraception. Free Links: OBGYN-10 OBGYN-101 Gray Haired Note Brookside Associates Medical Education Division
Mike Hughey, MD
about 9 years ago
Gestational Diabetes A transient, self-limiting, hyperglycaemia, which occurs during pregnancy due to maternal endocrine changes. Glucose Control Insulin cause…
over 9 years ago