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Case Study Acute Abdominal Pain 4 October 2010 By hybridmedic Leave a Comment Share/Bookmark Something thats been nagging

g me I had to write about The Case Its 3 am, you can tell that because the alarm clock by your bunk bed in the unlit bedhall says so. The chill of the air bites your nose as you try and go back to sleep. You close your eyes and roll over, but the crackle of the station intercom wakes you companies stand by followed by a high pitched beeping tone and the turnout lights coming on. Respond to a one alpha one, 35 year old female with abdominal pain Belly pain you grumble as you roll out of bed, pulling on your uniform pants and boots and walking out of the room. You grab the print out sheet from the watchman and head to your ambulance. You depress the button on the door opener as your ambulance roars to life and pulls out of the bay. This is a low priority call so you respond without lights or siren. The drive takes forever it seems, which seems to be a function of the time of day and not necessarily distance, but you finally arrive at your given address. You grab your first in bag and pull on some gloves on the way up to the door. You find your patient, a 35 year old woman, in the back bedroom of the small three bedroom house, she appears in obvious severe pain. She describes the onset of severe pain to be sudden, and woke her from sleep. She describes the pain as sharp and localized to the right upper quadrant (RUQ) that is unrelieved by positioning. She states she tried to drink something but only vomited it back up and the pain does not radiate as well as rating a 10 of 10 on a 0-10 scale. She is able to ambulate to the ambulance and you secure her to the cot. On palpation there is no rebound tenderness or masses noted, and the pain increases on palpation with muscle guarding. You initiate IV access and advise the patient to assume a position of comfort (she assumes a recumbent position on the right side). You place the monitor in a position to view it and dial your portable radio in the closest hospital Discussion

Acute non-traumatic abdominal pain is one the most common presentations to the ED, and similarly, emergency medical services calls for service, representing about 6% of ED visits (Jones et al, 2005). The causes are many, making an exact diagnosis of pain extremely difficult simply because of the wide array of organs in the abdominal cavity. It contains the organs necessary for blood filtering, blood sugar regulation, excess fluid elimination, and digestion of food and elimination of waste products. Outside of trauma, problems in the abdomen could range from inflammatory responses due to infections like PID, hepatitis, or appendicitis. Chronic inflammatory diseases like Crohns or ulcerative colitis are also common, or the problem could be mechanical such as bowel obstruction or hernia. Rarely there will be a vascular problem such as ischemia which leads to infarcted bowel. Bowel obstructions and bowel infarctions are commonly problems in the elderly due to decreased gastric motility and will often go unrecognized if those patients are institutionalized. All of these problems will cause a pain response. This a common problem faced by EMS and ED physicians alike: we dont treat pain adequately. This stems from the teachings of physicians stemming back decades. Dr Zachary Cope, in his book Early Diagnosis of the Acute Abdomen, printed in 1921, states that Though it may appear cruel, it is really kind to withhold morphine until one is certain or not that surgical interference is necessary, i.e. until a reasonable diagnosis has been made (Jones et al 2005). Physicians not only used this as a base to deny abdominal pain patients analgesics for anywhere from 2 to 6 hours because they may mask symptoms, but also as a crutch in favor of obtaining informed patient consent.

Recent studies have proven these beliefs to be false. In Radiology, Vermeulen et al stated in Acute Appendicitis: influence of early pain relief on the accuracy on clinical and US findings in the decision to operate, that they designed a double blind, placebo controlled study to challenge the belief that analgesia affected the assessment findings necessary to diagnose appendicitis. They admitted 340 patients to the study with 175 patients receiving morphine and 165 patients receiving placebo. The appropriateness of surgery vs discharge was 100% in all groups: placebo vs morphine, and men vs women. Wolfe et al in Morphine and Appendicitis also

Case Study Abdominal pain and High Calcium May 1, 2008 Back to Basics Ilan Gabriely, M.D., James P. Leu, M.D., and Uriel S. Barzel, M.D. A 41-year-old woman was brought by her husband to the emergency department with a history of 72 hours of epigastric pain, nausea, repeated vomiting, and altered mental status. Her blood calcium was found to be 18.9 mg per deciliter (4.7 mmol per liter). Hypercalcemia of this degree is a medical emergency. The patient with severe hypercalcemia is invariably dehydrated, and the first line of treatment should be vigorous hydration with intravenous normal saline with close observation of blood electrolytes and renal function. Additional treatment measures would depend on the cause of the hypercalcemia, the history, and the result of the workup. The patients husband reported that 4 days earlier they had returned from a vacation in Central America, where the patient had consumed a lot of alcohol. He noted that she was in her usual state of health until 3 days earlier, when she started having severe abdominal pain, followed by multiple episodes of vomiting. The patient had a history of peptic ulcer disease years before and still noted some occasional episodes of abdominal pain, which she had been treating with chewable antacid tablets containing calcium carbonate (Tums, GlaxoSmithKline). She also had a long history of chronic low back pain, which she treated with over-the-counter analgesics. A few months

earlier, she had been told by her primary care physician that she had a mildly elevated blood calcium level of 10.9 mg per deciliter (2.7 mmol per liter). Her physician was contacted and reported that her intact parathyroid hormone (PTH) blood level at her last examination was 33.9 pg per milliliter (normal range, 7 to 53). No further diagnostic studies were done. Medications at home included Tums as needed for abdominal pain and a multivitamin. Habitually, she had been drinking 2 to 3 shots of vodka and some wine daily. Her family history was negative for parathyroid disease, nephrolithiasis, and cancer. The history of a measurable PTH level in the face of elevated blood calcium suggests that the patient may have primary hyperparathyroidism, the most common cause of hypercalcemia. The level of hypercalcemia in this case, however, would be extremely rare with primary hyperparathyroidism; if it occurred, such a parathyroid crisis might require emergency parathyroidectomy. Given her history of low back pain, imaging studies should be obtained to evaluate the patient for lytic lesions from a malignant process. She should also be evaluated for other causes of hypercalcemia, including hyperthyroidism, vitamin D overdose, neoplasia, and granulomatous diseases. The patients reported alcohol use suggests the possibility that alcohol withdrawal may be contributing to her altered mental status, although the extreme hypercalcemia alone could account for her presentation. Close monitoring for withdrawal signs and symptoms is mandatory. Amylase and lipase should also be checked, given the possibility of alcohol-induced pancreatitis. On physical examination, the blood pressure was 160/90 mm Hg, the heart rate 100 beats per minute, and the temperature 37.4C. The patient was disoriented and intermittently writhing in pain. Her skin turgor was poor, and her oral mucosa was dry. The cardiac examination was significant only for tachycardia, and the pulmonary examination was normal. There was epigastric tenderness on palpation but no rebound tenderness. The patient was responsive to simple commands and was not tremulous. There were no other significant neurologic findings. The blood urea nitrogen was 13 mg per deciliter (4.6 mmol per liter); creatinine, 1.1 mg per deciliter (97 mol per liter); sodium, 137 mmol per

liter; potassium, 3.2 mmol per liter; chloride, 81 mmol per liter; bicarbonate, 37.2 mmol per liter; glucose, 96 mg per deciliter (5.3 mmol per liter); phosphorus, 2.0 mg per deciliter (0.65 mmol per liter); and magnesium, 1.2 mg per deciliter (0.49 mmol per liter). Blood tests for intact PTH, PTH-related protein, and 25-hydroxyvitamin D were performed. CLICK TO ENLARGE

The physical findings are consistent with the presence of a hypovolemic state. Other than the tachycardia, there are no other stigmata of alcohol withdrawal. However, it is unclear when the patient had her last drink, so prophylaxis for withdrawal may be warranted. Hypochloremia and alkalemia are probably due to persistent vomiting. The intravenous administration of normal saline at a rate of 200 ml per hour may reduce the level of blood calcium and provide sufficient chloride ion to allow for the correction of the hypochloremia and the alkalosis. The intact PTH level was undetectable. The lipase level was 1848 U per liter (normal range, 7 to 60), and the amylase level was 1354 U per liter (normal range, 40 to 128) (Table 1). The patient was treated with intravenous saline at a rate of 200 ml per hour, and prophylaxis for alcohol withdrawal with intravenous lorazepam was started. Intravenous morphine was given intermittently to alleviate abdominal pain. Before hyperparathyroidism can be ruled out, it is important to consider whether the hook effect may explain the undetectable PTH level. To identify an antigen, an immunoassay must contain an excess of the antibodies relative to the antigen. The hook effect refers to a situation in which the level of the circulating antigen is very high and thus the antibodies are fully bound, resulting in a severe underestimation of the hormone level. To overcome this problem, the assay must be carried out in multiple dilutions. Hypomagnesemia may impair the release of PTH and mask the presence of

hyperparathyroidism. The elevation of amylase and lipase confirms the suspicion of acute pancreatitis. The patient was treated with 2 g of intravenous magnesium gluconate. A repeat serum magnesium level was 1.7 mg per deciliter (0.70 mmol per liter). Intact PTH was again undetectable on repeated assays with dilutions. Computed tomography (CT) of the neck revealed no parathyroid masses. CT of the chest was normal. Abdominal CT showed an edematous pancreas with surrounding infiltration of the mesenteric fat, a finding consistent with acute pancreatitis. No bone lesions were noted on the chest or abdominal CT scans. The patients blood calcium level fell to 11.8 mg per deciliter (3.0 mmol per liter) by day 2 and to 8.5 mg per deciliter (2.1 mmol per liter) by day 3 with intravenous hydration alone, and the serum creatinine level fell to 0.7 mg per deciliter (62 mmol per liter). Her mental status slowly improved. The initial information that was obtained from the patients primary physician, which indicated a mildly elevated calcium level and an inappropriately normal PTH level, suggested mild primary hyperparathyroidism, but the currently suppressed intact PTH level appears inconsistent with this diagnosis. Insofar as primary hyperparathyroidism is associated with resetting of the calcium receptor to a higher set point, it is possible that the patient does have underlying primary hyperparathyroidism but that a second disorder has independently raised the calcium level and thus suppressed the PTH secretion. The rapid decline in the serum calcium level with intravenous hydration indicates that there is no need to consider urgent parathyroid surgery. The normalization of the very high calcium level with hydration also makes a number of other causes of hypercalcemia (such as solid tumors, hematopoietic tumors, granulomatous disease, and cancer metastatic to bone) less likely. Once the patients mental status improves further, a careful history of her diet and supplements should be obtained and evaluated for possible vitamin D and calcium overdose. The serum 25-hydroxyvitamin D level was 48 ng per deciliter (120 nmol per liter; normal range, 20 to 100 ng [50 to 250 nmol]). The level of PTH-related protein was normal. The serum calcium level remained normal after the intravenous fluids were discontinued. The patients mental status further

improved, and there was a gradual improvement in the clinical and laboratory markers of pancreatitis. The normal 25-hydroxyvitamin D level rules out vitamin D toxicity. The episode of acute pancreatitis could have been secondary to hypercalcemia or to alcohol excess. In response to further questioning, the patient reported that during the days before admission she had consumed the contents of entire containers of Tums and a preparation containing sodium bicarbonate (Alka-Seltzer, Bayer) because of the severe abdominal pain. She did not consume any other medications or supplements. Tums contains calcium carbonate, and Alka-Seltzer contains sodium bicarbonate. Hypercalcemia is an inevitable result of the intake of alkali and calcium in the context of dehydration and metabolic alkalosis. This history, together with the laboratory-test results, establishes the milk alkali syndrome as the primary diagnosis. Commentary Effective treatment for peptic ulcer disease was first introduced by Bertram Sippy1 in 1915. The Sippy regimen included hourly ingestion of milk and cream (and the gradual addition of eggs and cooked cereal) for 10 days, combined with the ingestion of alkaline powders. Although noncurative, this regimen provided some symptomatic relief.2 However, later reports showed serious toxicity associated with this regimen, including renal failure, alkalosis, and hypercalcemia, with normalization of all measures once the treatment was withdrawn.3 Over the next several decades, the milk alkali syndrome was frequently described, mostly in men with peptic ulcer disease who were receiving treatment with large amounts of calcium from milk and absorbable alkali.4 It proved fatal in some patients who had protracted vomiting due to secondary pyloric obstruction and who presented with hypovolemia, renal failure, alkalosis, and hypercalcemia. With the advent in recent years of better treatment options for peptic ulcer disease, the prevalence of the milk alkali syndrome has greatly declined.5 During the past 15 years, the milk alkali syndrome has been reported in patients without a history of peptic ulcer disease, most commonly in women taking calcium supplements at doses above the recommended range of 1200 to 1500 mg of elemental calcium daily for the prevention and treatment of

osteoporosis.5 Furthermore, calcium has been added to many over-thecounter products and supplements, such as fast-acting antacids, vitamin preparations, juices, and even acetaminophen, which has provided multiple opportunities for inadvertent excessive intake of calcium by consumers. The pathogenesis of the milk alkali syndrome involves a reduction in the ability of the kidney to excrete excess calcium. This reduction is secondary to a decrease in the glomerular filtration rate (due to renal vasoconstriction and hypovolemia) and to a significant increase in tubular reabsorption of calcium (secondary to metabolic alkalosis).6 The plasma PTH level decreases with the rise in the serum calcium level. Thus, the constellation of excess oral intake of calcium and milk, plus impaired renal function, may result in PTH suppression, hypercalcemia, and hyperphosphatemia. In cases of chronic ingestion of excessive alkaline calcium preparations and milk, metastatic calcifications and occasionally nephrocalcinosis may occur,7 whereas such complications are not expected with acute milk alkali syndrome, as in the present case. The most important clue to the diagnosis of the milk alkali syndrome is a history of excessive calcium and alkali intake. Many patients do not consider over-the-counter preparations as medications and therefore do not report taking calcium supplements. Conversely, physicians may fail to identify certain over-the-counter preparations or supplements as a significant source of calcium. Hence, a detailed history attending to diet and supplement intake is critical. Hypercalcemia, metabolic alkalosis, and impaired renal function are classic laboratory findings in patients with the milk alkali syndrome.8 Hyperphosphatemia, hypophosphaturia, and hypercalciuria may also be present, depending on the cause of the milk alkali syndrome. (For example, hyperphosphatemia is common in patients who have ingested excessive amounts of milk and calcium carbonate, whereas hyperphosphatemia does not generally develop in patients with an excessive intake of calcium carbonate alone.) The documentation of low levels of intact PTH in patients with hypercalcemia is helpful in the diagnosis of the milk alkali syndrome,9 since this finding indicates that primary hyperparathyroidism cannot explain the hypercalcemia. When parathyroid function is normal, the plasma PTH level varies inversely with the plasma calcium level. Once excess calcium intake is

stopped and the serum calcium level normalizes, plasma PTH may rebound. Reports indicate that the rebound in PTH level occurs rapidly (within hours) when excess calcium intake is stopped and the patient is vigorously hydrated and that the intact PTH level reaches a peak at 7 days.10 Intact PTH levels may be transiently elevated during this phase in patients who have an abrupt decrease (overcorrection) in blood calcium levels. Thus, it is critical that any intact PTH level be correlated with simultaneous blood calcium levels. In conclusion, the milk alkali syndrome, which was commonly seen four decades ago in men, seems to be increasingly prevalent, probably because of the increased use of over-the-counter calcium preparations and supplements by women.10 A basic tenet of medical care is that a complete history is often the key to diagnosis. This is clearly true for the present case, in which the correct diagnosis depended on a history of excess calcium and alkali intake in a dehydrated and alkalotic patient, supported by the documentation of a normal 25-hydroxyvitamin D level and a suppressed level of intact PTH. Pregnancy Induced Hypertension (PIH) is a condition in which vasospasms occur during pregnancy in both small and large arteries. Signs of hypertension, proteinuria, and edema develop. It is unique to pregnancy and occurs in 5% to 7% of pregnancies in the united states. Despite years of research, the cause of the disorder is still unknown. Originally it was called toxemia because researchers pictured a toxin of some kind being produced by a women in response to foreign protein of the growing fetus, the toxin leading to the topical symptoms. No such toxins have ever been identified. A condition separate from chronic hypertension, PIH tends to occur most frequently in women of color or with a multiple pregnancy; primiparas are younger than 20 years of age or older than 40 years, women from low socio economic backgrounds, those who have an underlying disease such as heart disease, diabetes with vessel or renal involvement and essential hypertension. PIH is classified as gestational hypertension, mild preeclampsia, severe preeclampsia and eclampsia, depending on how far development advances. Gestational hypertension when develops an elevated blood pressure but has no proteinuria or edema. Perinatal mortality is not increased with simple gestational hypertension, so no drug therapy is necessary; and blood pressure returns to normal after birth. Mild preeclampsia when blood pressure rises to 140/90 mmHg or systolic pressure elevated 15 mmHg above pregnancy level; mild edema in upper extremities or face. Severe preeclampsia when blood pressure has risen to 160 mmHg systolic and 110 mmHg diastolic; proteinuria; pulmonary or cardiac involvement; extensive

peripheral edema; hepatic dysfunction; theombocytopenia. Eclampsia is the most severe classification of PIH and seizure or coma Accompanied by s/s of preeclampsia. Any woman who falls into one of the high-risk categories for PIH should be observed carefully for symptoms at prenatal visits. She needs instructions about what symptoms to watch for so she can alert her clinician if additional symptoms occur between visits. Anatomy and Physiology: When most people hear the term cardiovascular system, they immediately think of the heart. We have all felt our own heart "pound" from time to time, and we tend to get a bit nervous when this happens. The crucial importance of the heart has been recognized for a long time. However, the cardiovascular system is much more than just the heart, and from a scientific and medical standpoint, it is important to understand why this system is so vital to life. Most simply stated, the major function of the cardiovascular system is transportation. Using blood as the transport vehicle, the system carries oxygen, nutrients, cell wastes, hormones, and many other substances vital for body homeostasis to and from the cells. The force to move the blood around the body is provided by the beating heart. The cardiovascular system can be compared to a muscular pump equipped with one-way valves and a system of large and small plumbing tubes within which the blood travels. HEART: The heart is a muscular organ found in all vertebrates that is responsible for pumping blood throughout the blood vessels by repeated, rhythmic contractions. The heart is enclosed in a double-walled sac called the pericardium. The superficial part of this sac is called the fibrous pericardium. This sac protects the heart, anchors its surrounding structures, and prevents overfilling of the heart with blood. It is located anterior to the vertebral column and posterior to the sternum. The size of the heart is about the size of a fist and has a mass of between 250 grams and 350 grams. The heart is composed of three layers, all of which are rich with blood vessels. The superficial layer, called the visceral layer, the middle layer, called the myocardium, and the third layer which is called the endocardium. The heart has four chambers, two superior atria and two inferior ventricles. The atria are the receiving chambers and the ventricles are the discharging chambers. The pathway of blood through the heart consists of a pulmonary circuit and a systemic circuit. Blood flows through the heart in one direction, from the atrias to the ventricles, and out of the great arteries, or the aorta for example. This is done by four valves which are the tricuspid atrioventicular valve, the mitral atrioventicular valve, the aortic semilunar valve, and the pulmonary

semilunar valve. Systemic circulation is the portion of the cardiovascular system which carries oxygenated blood away from the heart, to the body, and returns deoxygenated blood back to the heart. The term is contrasted with pulmonary circulation. Pulmonary circulation is the portion of the cardiovascular system which carries oxygen-depleted blood away from the heart, to the lungs, and returns oxygenated blood back to the heart. The term is contrasted with systemic circulation. A separate system known as the bronchial circulation supplies blood to the tissue of the larger airways of the lung. Arteries are blood vessels that carry blood away from the heart. All arteries, with the exception of the pulmonary and umbilical arteries, carry oxygenated blood. Pulmonary arteries The pulmonary arteries carry deoxygenated blood that has just returned from the body to the heart towards the lungs, where carbon dioxide is exchanged for oxygen. Systemic arteries Systemic arteries can be subdivided into two types muscular and elastic according to the relative compositions of elastic and muscle tissue in their tunica media as well as their size and the makeup of the internal and external elastic lamina. The larger arteries (>10mm diameter) are generally elastic and the smaller ones (0.1-10mm) tend to be muscular. Systemic arteries deliver blood to the arterioles, and then to the capillaries, where nutrients and gasses are exchanged. The Aorta The aorta is the root systemic artery. It receives blood directly from the left ventricle of the heart via the aortic valve. As the aorta branches, and these arteries branch in turn, they become successively smaller in diameter, down to the arteriole. The arterioles supply capillaries which in turn empty into venules. The very first branches off of the aorta are the coronary arteries, which supply blood to the heart muscle itself. These are followed by the branches off the aortic arch, namely the brachiocephalic artery, the left common carotid and the left subclavian arteries. Aorta the largest artery in the body, originating from the left ventricle of the heart and extends down to the abdomen, where it branches off into two smaller arteries (the common iliacs). The aorta brings oxygenated blood to all parts of the body in the systemic circulation. The aorta is usually divided into five segments/sections: Ascending aortathe section between the heart and the arch of aorta Arch of aortathe peak part that looks somewhat like an inverted "U"

Descending aortathe section from the arch of aorta to the point where it divides into the common iliac arteries o Thoracic aortathe half of the descending aorta above the diaphragm o Abdominal aortathe half of the descending aorta below the diaphragm Arterioles Arterioles, the smallest of the true arteries, help regulate blood pressure by the variable contraction of the smooth muscle of their walls, and deliver blood to the capillaries. Veins are blood vessels that carry blood towards the heart. Most veins carry deoxygenated blood from the tissues back to the lungs; exceptions are the pulmonary and umbilical veins, both of which carry oxygenated blood. Veins differ from arteries in structure and function; for example, arteries are more muscular than veins and they carry blood away from the heart. Veins are classified in a number of ways, including superficial vs. deep, pulmonary vs. systemic, and large vs. small. Superficial veins Superficial veins are those whose course is close to the surface of the body, and have no corresponding arteries. Deep veins Deep veins are deeper in the body and have corresponding arteries. Pulmonary veins The pulmonary veins are a set of veins that deliver oxygenated blood from the lungs to the heart. Systemic veins Systemic veins drain the tissues of the body and deliver deoxygenated blood to the heart. Atrium sometimes called auricle, refers to a chamber or space. It may be the atrium of the lateral ventricle in the brain or the blood collection chamber of a heart. It has a thin-walled structure that allows blood to return to the heart. There is at least one atrium in animals with a closed circulatory system. Right atrium is one of four chambers (two atria and two ventricles) in the human heart. It receives deoxygenated blood from the superior and inferior vena cava and the coronary sinus, and pumps it into the right ventricle through the tricuspid valve. Attached to the right atrium is the right auricular appendix. Left atrium is one of the four chambers in the human heart. It receives oxygenated blood from the pulmonary veins, and pumps it into the left ventricle, via the atrioventricular valve. Ventricle is a chamber which collects blood from an atrium (another heart

chamber that is smaller than a ventricle) and pumps it out of the heart. Right ventricle is one of four chambers (two atria and two ventricles) in the human heart. It receives deoxygenated blood from the right atrium via the tricuspid valve, and pumps it into the pulmonary artery via the pulmonary valve and pulmonary trunk. Left ventricle is one of four chambers (two atria and two ventricles) in the human heart. It receives oxygenated blood from the left atrium via the mitral valve, and pumps it into the aorta via the aortic valve. Pathophysiology of Pregnancy Induced Hypertension (PIH): Clinical Manifestations: A. Mild Preeclampsia BP of 140/90 1+ to 2+ proteinuria on random weight gain of 2 lbs per week on the 2nd trimester and 1 lb per week on the 3rd trimester Slight edema in upper extremities and face B. Severe Preeclampsia BP of 160/110 3-4+ protenuria on random Oliguria (less than 500 ml/24 hrs) Cerebral or visual disturbances Epigastric pain Pulmonary edema Peripheral edema Hepatic dysfunction C. Eclampsia is an extension of preeclampsia and is characterized by the client experiencing seizures. Diagnostic Evaluation: 1. Based on the presenting symptoms. Often the disease process has been developing and affecting the renal and vascular system 2. Frequently a sudden weight gain will occur, of 2 lb. or more in 1 week, or 6 lb. or more within 1 month. This often occurs before the edema is present. Medical Treatment and Evaluation: 1. Magnesium Sulfate (Pregnancy risk category B) muscle relaxant, prevent seizures loading dose 4-6g, maintenance dose 1-2g/h IV infuse IV dose slowly over 15-30 min. Always administer as a piggy back infusion.

Assess PR, urine output, DTR, and clonus every hour. Observe for CNS depression and hypotonia in infant at birth. 2. Hydrazaline (Apresoline) Pregnancy risk category C anti hypertensive (peripheral vasodilator) use to decrease hypertension 5-10mg/IV Administer slowly to avoid sudden fall of BP Maintain diastolic pressure over 90 mmHg to ensure adequate placental filling. 3. Diazepam (Valium) Pregnancy risk category D halt seizures 5-10mg/IV administer slowly. Dose may be repeated every 10-15 min. (up to 30mg/hr) Observe for respiratory depression for both mother and infant at birth. 4. Calcium Gluconate (Pregnancy risk category C) antidote for Magnesium Sulfate 1g/IV (10 mL of a 10% solution) have prepared at bed side when administering Magnesium Sulfate administer at 5mL/min. Complications of PIH: 1. Intrauterine growth restriction (IUGR) an abnormally restricted symmetric or asymmetric growth of fetus 2. Oligohydramnios abnormally low volume of amniotic fluid 3. Risk of placental abruption premature separation of a normally situated placenta from the wall of uterus 4. Risk of preterm delivery (often iatrogenic) delivery before 37 weeks of gestation 5. Coagulopathy 6. Stillbirth 7. Seizures 8. Coma 9. Renal failure 10.Maternal hepatic damage 11.Hemolysis 12.Elevated liver enzymes levels 13.Low platelet count (HELLP syndrome) Nursing Interventions: Intervention for mild Rationale: PIH:

1. Assess maternal VS and -to detect any increase which is fetal heart rate. warning that a womens condition is worsening. 2. Encourage elevation of -to increase venous blood return. edematous arms and legs. 3. Encourage compliance -to increase evacuation of sodium and with bed rest in a lateral encouraging diuresis and lateral recumbent position. recumbent position can avoid uterine pressure on the vena cava and prevent supine hypotension syndrome. 4. Provide emotional -this can make a women support. underestimate the severity of the situation. 5. Support patient with -because a bright light can trigger bed rest and darken the seizures. room if possible. 6. Obtain daily hematocrit -to monitor blood concentration and levels as ordered. help to the extent of plasma loss to interstitial space or extent of the edema. 7. Obtain blood studies -to assess for renal and liver function (CBC, platelets count, and the development of disseminated liver function, BUN and intravascular coagulation which often creatinine, and fibrin accompanies severe vasospasms. degregation). 8. Obtain daily weights at -to evaluate tissue fluid retention. the same time each day. 9. Raise side rails. -to help prevent injury if seizure should occur. 10. Support nutritious diet -to compensate for protein she is of moderate to high in losing in her urine. protein and moderate in sodium. 11. An indwelling catheter -to allow accurate recording of may be inserted as output and comparison with intake. ordered. 12. Oxygen -to maintain adequate fetal administration to the oxygenation and prevent fetal

mother may be given as bradycardia. ordered. 13. Administer medication -to prevent seizures and for seizures and hypertension. hypertension episodes as ordered. Intervention for severe PIH: 1. Maintain patients airway by not putting a tongue blade between a womens teeth during seizures. 2. Turn a woman on her side. Rationale: -to prevent broken of teeth which could then be aspirated.

-to allow secretions to drain from her mouth.

Discharge Plan: Exercise 1. encourage patients on deep breathing exercises. 2. move extremities when lying. 3. elevate the head part when sleeping, to promote increase peripheral circulation 4. encourage overall passive and active exercises program during pregnancy to prevent need for cesarean birth. 5. exercises like tailor sitting, squatting, kegel exercise, pelvic rocking, and abdominal muscle contraction will promote easy delivery. Treatment: 1. use of drugs 2. catheterization 3. obtaining labs. (CBC, platelets count, liver function, BUN and creatinine, and fibrin degregation) Health Teaching: 1. Encourage patient foe sodium restriction. 2. Encourage to avoid foods rich in oil and fats. 3. Encourage patient to limit her daily activities and exercises. Ongoing Assessment: 1. Observe carefully for symptoms at prenatal visit.

2. Give instruction about what symptoms to watch for so she can alert her clinician if additional symptoms occur between visits. Diet: 1. low fats and sodium diet, restriction if possible. 2. high in protein, calcium and iron. 3. Adequate fluid intake Sex: 1. limit sexual activity 2. sexual intercourse at 2nd trimester should be avoided.

sample case study for hypertension Although numerous people do not realize it, hypertension and high cholesterol have been discovered to be associated to one another. There are many issues that can be induced by high blood pressure that had their roots in another issue. For example, high cholesterol levels can lead to high blood pressure, which in turn may result in heart attacks, stroke or a great many other problems such as an arterial blood vessel condition. The U.S. is just one location that the problem is worsening as people live such dormant lifestyles, which is getting more common everyday in the diagnosing of high blood pressure, artery and cardiac complaints and assorted other draining complaints. The truth is, individuals eat more than they ought to, they eat the inappropriate foods and dont work out to hold their weight down. When you suffer with high bloodpressure your heart literally works itself to destruction and cholesterol is one of the reasons for hypertension. When the LDL cholesterol is raised and the HDL cholesterol is low you are in peril of developing heart condition. The continuous elevated heart rate makes it work too hard over a prolonged time period and eventually it will just stop working. What takes place when an individual has a heart attack is that fundamentally the heart has been worked to hard, to the level that it cannot function any longer. The liver produces cholesterol so if you are contributing to that with the nutrients you take, the cholesterol levels will become extremely high. This can result in heart complaint when the arteries become clogged with calcium, cholesterol and fatty acids which successively results in the arterial blood vessels becoming smaller, so the heart works harder to pump the blood through. There are in addition other reasons for high blood pressure though for example: diabetes, cancerous tumors, kidney complaint but sodium, genetics,

caffeine, alcohol and obesity are all contributing components. Stress is another cause of hypertension, nonetheless, the most usual cause is hypertension and high cholesterol when the diagnosis of other lasting sickness is not named. Keeping a propercholesterol level is not as hard as you may believe if you eat healthily and workout on a regular basis these are the primary methods to reduce cholesterol levels. This is an superb tradeoff when you study the benefits of staying healthy and keeping from developing hypertension which in turn will lead to other problems. You cannot completely take cholesterol out of the picture because it is necessary for your cells to function in the proper way. The key to controlling cholesterol is to not over consume it and keep the levels within a regular range, so consuming fast food day in and day out will raise cholesterol levels. As well as consuming vegetables, fruits, grains and solid foods with low sodium levels, leave alone those with high fat. The idea is long term habits which will keep you from acquiring hypertension and high cholesterol in addition to better your wellbeing, so all you must do is watch your diet and do some type of work out about four times each week.

Diabetes Mellitus Case Study INTRODUCTION: Diabetes mellitus is a condition in which the pancreas no longer produces enough insulin or cells stop responding to the insulin that is produced, so that glucose in the blood cannot be absorbed into the cells of the body. Symptoms include frequent urination, lethargy, excessive thirst, and hunger. The treatment includes changes in diet, oral medications, and in some cases, daily injections of insulin. The most common form of diabetes is Type II, It is sometimes called age-onset or adult-onset diabetes, and this form of diabetes occurs most often in people who are overweight and who do not exercise. Type II is considered a milder form of diabetes because of its slow onset (sometimes developing over the course of several years) and because it usually can be controlled with diet and oral medication. The consequences of uncontrolled and untreated Type II diabetes, however, are the just as serious as those for Type I. This form is also called noninsulin-dependent diabetes, a term that is somewhat misleading. Many people with Type II diabetes can control the condition with diet and oral medications, however, insulin injections are sometimes necessary if treatment with diet and oral medication is not working.

The causes of diabetes mellitus are unclear, however, there seem to be both hereditary (genetic factors passed on in families) and environmental factors involved. Research has shown that some people who develop diabetes have common genetic markers. In Type I diabetes, the immune system, the bodys defense system against infection, is believed to be triggered by a virus or another microorganism that destroys cells in the pancreas that produce insulin. In Type II diabetes, age, obesity, and family history of diabetes play a role. In Type II diabetes, the pancreas may produce enough insulin, however, cells have become resistant to the insulin produced and it may not work as effectively. Symptoms of Type II diabetes can begin so gradually that a person may not know that he or she has it. Early signs are lethargy, extreme thirst, and frequent urination. Other symptoms may include sudden weight loss, slow wound healing, urinary tract infections, gum disease, or blurred vision. It is not unusual for Type II diabetes to be detected while a patient is seeing a doctor about another health concern that is actually being caused by the yet undiagnosed diabetes. Individuals who are at high risk of developing Type II diabetes mellitus include people who: are obese (more than 20% above their ideal body weight) have a relative with diabetes mellitus belong to a high-risk ethnic population (African-American, Native American, Hispanic, or Native Hawaiian) have been diagnosed with gestational diabetes or have delivered a baby weighing more than 9 lbs (4 kg) have high blood pressure (140/90 mmHg or above) have a high density lipoprotein cholesterol level less than or equal to 35 mg/dL and/or a triglyceride level greater than or equal to 250 mg/dL have had impaired glucose tolerance or impaired fasting glucose on previous testing Diabetes mellitus is a common chronic disease requiring lifelong behavioral and lifestyle changes. It is best managed with a team approach to empower the client to successfully manage the disease. As part of the team the, the nurse plans, organizes, and coordinates care among the various health disciplines involved; provides care and education and promotes the clients health and well being. Diabetes is a major public health worldwide. Its complications cause many devastating health problems. ANATOMY AND PHYSIOLOGY: Every cell in the human body needs energy in order to function. The bodys primary energy source is glucose, a simple sugar resulting from the digestion

of foods containing carbohydrates (sugars and starches). Glucose from the digested food circulates in the blood as a ready energy source for any cells that need it. Insulin is a hormone or chemical produced by cells in the pancreas, an organ located behind the stomach. Insulin bonds to a receptor site on the outside of cell and acts like a key to open a doorway into the cell through which glucose can enter. Some of the glucose can be converted to concentrated energy sources like glycogen or fatty acids and saved for later use. When there is not enough insulin produced or when the doorway no longer recognizes the insulin key, glucose stays in the blood rather entering the cells.

PATHOPHYSIOLOGY:

Image Source: www.caninsulin.com/Pathophysiology-algorithm.htm DIAGNOSTIC TEST: Several blood tests are used to measure blood glucose levels, the primary test for diagnosing diabetes. Additional tests can determine the type of diabetes and its severity. Random blood glucose test for a random blood glucose test, blood can be drawn at any time throughout the day, regardless of when the person last ate. A random blood glucose level of 200 mg/dL (11.1 mmol/L) or higher in persons who have symptoms of high blood glucose (see Symptoms above) suggests a diagnosis of diabetes. Fasting blood glucose test fasting blood glucose testing involves measuring blood glucose after not eating or drinking for 8 to 12 hours (usually overnight). A normal fasting blood glucose level is less than 100

mg/dL. A fasting blood glucose of 126 mg/dL (7.0 mmol/L) or higher indicates diabetes. The test is done by taking a small sample of blood from a vein or fingertip. It must be repeated on another day to confirm that it remains abnormally high (see Criteria for diagnosis below). Hemoglobin A1C test (A1C) The A1C blood test measures the average blood glucose level during the past two to three months. It is used to monitor blood glucose control in people with known diabetes, but is not normally used to diagnose diabetes. Normal values for A1C are 4 to 6 percent (show figure 3). The test is done by taking a small sample of blood from a vein or fingertip. Oral glucose tolerance test Oral glucose tolerance testing (OGTT) is the most sensitive test for diagnosing diabetes and pre-diabetes. However, the OGTT is not routinely recommended because it is inconvenient compared to a fasting blood glucose test. The standard OGTT includes a fasting blood glucose test. The person then drinks a 75 gram liquid glucose solution (which tastes very sweet, and is usually cola or orange-flavored). Two hours later, a second blood glucose level is measured. Oral glucose tolerance testing is routinely performed at 24 to 28 weeks of pregnancy to screen for gestational diabetes; this requires drinking a 50 gram glucose solution with a blood glucose level drawn one hour later. For women who have an abnormally elevated blood glucose level, a second OGTT is performed on another day after drinking a 100 gram glucose solution. The blood glucose level is measured before, and at one, two, and three hours after drinking the solution. MEDICATIONS: When diet, exercise and maintaining a healthy weight arent enough, you may need the help of medication. Medications used to treat diabetes include insulin. Everyone with type 1 diabetes and some people with type 2 diabetes must take insulin every day to replace what their pancreas is unable to produce. Unfortunately, insulin cant be taken in pill form because enzymes in your stomach break it down so that it becomes ineffective. For that reason, many people inject themselves with insulin using a syringe or an insulin peninjector,a device that looks like a pen, except the cartridge is filled with insulin. Others may use an insulin pump, which provides a continuous supply of insulin, eliminating the need for daily shots. The most widely used form of insulin is synthetic human insulin, which is chemically identical to human insulin but manufactured in a laboratory. Unfortunately, synthetic human insulin isnt perfect. One of its chief failings is that it doesnt mimic the way natural insulin is secreted. But newer types of

insulin, known as insulin analogs, more closely resemble the way natural insulin acts in your body. Among these are lispro (Humalog), insulin aspart (NovoLog) and glargine (Lantus). A number of drug options exist for treating type 2 diabetes, including: Sulfonylurea drugs. These medications stimulate your pancreas to produce and release more insulin. For them to be effective, your pancreas must produce some insulin on its own. Second-generation sulfonylureas such as glipizide (Glucotrol, Glucotrol XL), glyburide (DiaBeta, Glynase PresTab, Micronase) and glimepiride (Amaryl) are prescribed most often. The most common side effect of sulfonylureas is low blood sugar, especially during the first four months of therapy. Youre at much greater risk of low blood sugar if you have impaired liver or kidney function. Meglitinides. These medications, such as repaglinide (Prandin), have effects similar to sulfonylureas, but youre not as likely to develop low blood sugar. Meglitinides work quickly, and the results fade rapidly. Biguanides. Metformin (Glucophage, Glucophage XR) is the only drug in this class available in the United States. It works by inhibiting the production and release of glucose from your liver, which means you need less insulin to transport blood sugar into your cells. One advantage of metformin is that is tends to cause less weight gain than do other diabetes medications. Possible side effects include a metallic taste in your mouth, loss of appetite, nausea or vomiting, abdominal bloating, or pain, gas and diarrhea. These effects usually decrease over time and are less likely to occur if you take the medication with food. A rare but serious side effect is lactic acidosis, which results when lactic acid builds up in your body. Symptoms include tiredness, weakness, muscle aches, dizziness and drowsiness. Lactic acidosis is especially likely to occur if you mix this medication with alcohol or have impaired kidney function. Alpha-glucosidase inhibitors. These drugs block the action of enzymes in your digestive tract that break down carbohydrates. That means sugar is absorbed into your bloodstream more slowly, which helps prevent the rapid rise in blood sugar that usually occurs right after a meal. Drugs in this class include acarbose (Precose) and miglitol (Glyset). Although safe and effective, alpha-glucosidase inhibitors can cause abdominal bloating, gas and diarrhea. If taken in high doses, they may also cause reversible liver damage. Thiazolidinediones. These drugs make your body tissues more sensitive to insulin and keep your liver from overproducing glucose. Side effects of thiazolidinediones, such as rosiglitazone (Avandia) and pioglitazone hydrochloride (Actos), include swelling, weight gain and fatigue. A far more serious potential side effect is liver damage. The thiazolidinedione troglitzeone (Rezulin) was taken off the market in March 2000 because it caused liver

failure. If your doctor prescribes these drugs, its important to have your liver checked every two months during the first year of therapy. Contact your doctor immediately if you experience any of the signs and symptoms of liver damage, such as nausea and vomiting, abdominal pain, loss of appetite, dark urine, or yellowing of your skin and the whites of your eyes (jaundice). These may not always be related to diabetes medications, but your doctor will need to investigate all possible causes. Drug combinations. By combining drugs from different classes, you may be able to control your blood sugar in several different ways. Each class of oral medication can be combined with drugs from any other class. Most doctors prescribe two drugs in combination, although sometimes three drugs may be prescribed. Newer medications, such as Glucovance, which contains both glyburide and metformin, combine different oral drugs in a single tablet. NURSING INTERVENTIONS: Advice patient about the importance of an individualized meal plan in meeting weekly weight loss goals and assist with compliance. Assess patients for cognitive or sensory impairments, which may interfere with the ability to accurately administer insulin. Demonstrate and explain thoroughly the procedure for insulin selfinjection. Help patient to achieve mastery of technique by taking step by step approach. Review dosage and time of injections in relation to meals, activity, and bedtime based on patients individualized insulin regimen. Instruct patient in the importance of accuracy of insulin preparation and meal timing to avoid hypoglycemia. Explain the importance of exercise in maintaining or reducing weight. Advise patient to assess blood glucose level before strenuous activity and to eat carbohydrate snack before exercising to avoid hypoglycemia. Assess feet and legs for skin temperature, sensation, soft tissues injuries, corns, calluses, dryness, hair distribution, pulses and deep tendon reflexes. Maintain skin integrity by protecting feet from breakdown. Advice patient who smokes to stop smoking or reduce if possible, to reduce vasoconstriction and enhance peripheral flow.

Ectopic pregnancy

What is an ectopic pregnancy? It's a pregnancy that develops outside the womb, usually in one of the fallopian tubes. That is why it is also known as a tubal pregnancy. It happens in about two of every 100 pregnancies in India. As the pregnancy grows, it causes pain and bleeding and, if not recognized, the tube can rupture, causing internal bleeding. This is a medical emergency and can be fatal. The pregnancy itself never survives -- it can't be moved to the womb and has to be removed. When is it likely to happen? An ectopic is most commonly found between the fourth and tenth week of pregnancy -- usually from weeks five to seven. Why does it happen? The fertilised egg normally spends four to five days travelling down the tube from the ovary to the womb where it implants and begins to develop. The most common reason for an ectopic pregnancy is when the fallopian tube has been damaged, and this causes a blockage or narrowing which prevents the egg from reaching its destination. Instead, it implants in the wall of the tube. In a few cases, the egg implants in an ovary, in the cervix, directly in the abdomen, or even in an earlier c-section scar. In rare cases, a woman may have a normal pregnancy in her uterus and an ectopic pregnancy at the same time. This is called a heterotopic pregnancy and it's more likely to happen if you've had fertility treatments, such as in-vitro fertilisation. Who is at risk? An ectopic pregnancy can happen to any woman, but there are circumstances, which make it more likely. These might include: If you've had pelvic inflammatory disease (which is most often caused by the sexually transmitted infection chlamydia or or gonorrhoea) as this can cause

damage and scarring to the fallopian tubes. Some experts believe that up to half of all ectopic pregnancies are related to the chlamydia infection. Experts also believe that if chlamydia has affected your fallopian tubes then your risk of an ectopic pregnancy is much increased. If you have tubal endometriosis. You may be more at risk because this increases the risk of scarring. If you've had any abdominal surgery, including an appendix removal or a caesarian section. If you have a contraceptive coil fitted. While this will prevent a pregnancy in the womb, it's less effective at preventing one in the tube. If you are taking the contraceptive mini-pill. This has been associated with a slightly higher rate of ectopic pregnancy. If you've had a previous ectopic pregnancy. If you are over 35. What are the symptoms? One-sided pain in the lower abdomen that is severe and persistent is the most common symptom. Many women describe it as an intense stabbing pain. Any woman who experiences this and who could possibly be pregnant should see a doctor. Collapse, preceded by feeling faint, dizziness, diarrhoea, vomiting and/or pain. Vaginal bleeding. You might not know that you're pregnant and mistake this for a period, but the blood is usually different from a normal period - often

dark and watery. Shoulder-tip pain. This can happen if there is internal bleeding which irritates other internal body organs, such as the diaphragm. Pain in the lower back Pain when having a wee or opening your bowels. What should I do? If you have any of these symptoms, go to hospital right away. You're likely to be referred for an ultrasound examination and a sensitive pregnancy test (unless the tube has ruptured, in which case you'll go straight to surgery). The scan may be done using an intravaginal probe, as the pregnancy may not show up using an abdominal scan. You might also have a blood hormone test if the scan isn't conclusive. How is it treated? If an ectopic pregnancy is suspected you will probably be taken to theatre for a laparoscopic examination (where a narrow viewing instrument is put into your abdomen through a tiny cut) to inspect your tubes. If an ectopic is discovered, the surgeon can remove this using the laparoscope to cut the tube and remove the pregnancy, leaving the tube intact. If the tube has ruptured, sometimes abdominal surgery is needed rather than laparoscopic surgery (although not always) to remove the pregnancy and tubal damage. In some cases, a blood transfusion may be needed to replace lost blood. In some hospitals the drug methotrexate, which terminates the pregnancy, can be used instead of surgery. This treatment is most effective in very early

pregnancy and it can be used where there is no bleeding and the tube has not ruptured. The pregnancy is lost and reabsorbed by the mother, who will then experience bleeding for a couple of weeks. Methotrexate may also be used if the ectopic is picked up very early on and the levels of the pregnancy hormone HCG are still fairly low. However, do let your doctor know if you are breastfeeding an older child or if you have certain health conditions. In such cases, your doctor may not prescribe the medicine and would look at other options, which may include surgery. Note: If your blood is Rh-negative, you'll need a shot of Rh immunoglobulin after being treated for an ectopic pregnancy (unless the baby's father is also Rh negative). Will it affect my fertility? The answer to this is yes, possibly. If your fallopian tubes are undamaged after an ectopic pregnancy, then your chances of conceiving again remain the same. If one of the tubes ruptured or was badly damaged, your chances of conceiving again are reduced. Up to ten per cent of women may become infertile after an ectopic. Some 65 per cent of women will conceive again within 18 months of an ectopic, but if both your fallopian tubes were damaged or ruptured, you may need to think about IVF treatment. What are the chances of having another ectopic? There's about a 10 per cent risk of having another one. However, the risk is difficult to generalise about because of the differences in individual circumstances and the extent of the damage that takes place. That means that your overall chances of having a normal pregnancy next time around are still high.

You should arrange for a follow up appointment and ask for clear advice about your own future pregnancies from a consultant obstetrician. There is little you can do to prevent an ectopic pregnancy from happening in the future, although if your ectopic has been caused by a current chlamydia infection you can have a course of antibiotics to clear it up and reduce further damage to your tubes. When you do become pregnant again, see your doctor as soon as you can as you would be referred to an early pregnancy unit for a scan to check that your pregnancy is developing in the right place. How long should I wait before trying for another? Normally women who've had a laparoscopy are advised to wait three to four months before trying to conceive again. If you have had abdominal surgery, it's best to wait for six months to allow scarring to heal. Case study of an ectopic pregnancy Vinita, 37, has two children: Rahul is eight and Ila is five. 'I was 30 when I had my ectopic pregnancy. I already had a son of 16 months, so it was a shock when it happened. I didn't realise I was pregnant at first, as I've always had irregular cycles, and when I started bleeding after eight weeks I just thought it was a heavier period than usual. Before that I'd already done three pregnancy tests, all of which were negative. Shortly after this I had severe cramping pains, and then at work two days later, I collapsed. When I arrived at hospital, I began bleeding heavily and I was sent for a laparoscopy, where they had to remove my left tube as it had ruptured. My left ovary had to be removed, too. Fortunately the other tube and ovary were left intact.

It took about six weeks to recover and I found it all difficult to come to terms with -- thankfully my doctor and family helped me cope with it. I never found out what had caused it. Seven months later, I became pregnant with my daughter. I had a scan at five weeks to check the egg was in the right place and fortunately it was. However, I didn't relax until my baby was safely in my arms.'

CASE STUDY 3.2: VAGINAL BLEEDING DURING LATER PREGNANCY DIRECTIONS Read and analyze this case study individually. When the others in your group have finished reading it, answer the case study questions. Consider the steps in clinical decision-making as you answer the questions. The other groups in the room are working on the same or a similar case study. When all groups have finished, we will discuss the case studies and the answers each group has developed. CASE STUDY Mrs. C., who is 32 weeks pregnant, gravida three, has two healthy children. She has attended antenatal clinic regularly and all findings were within normal limits until her clinic visit 10 days ago. At that visit her blood pressure was noted to be 120/96 mm Hg; there were no other signs or symptoms of pregnancy-induced hypertension. Mrs. C. was counseled about danger signs and what to do if they occur and asked to return to the clinic in 2 weeks. She presents at the district hospital 2 days before her next clinic visit, accompanied by her mother-in-law, with vaginal bleeding, abdominal pain and a bad headache. ASSESSMENT (History, Physical Examination, Screening Procedures/Laboratory Tests) 1. What will you include in your initial assessment of Mrs. C., and why?

2. What particular aspects of Mrs. C.'s physical examination will help you make a diagnosis and identify her problems/needs, and why? 3. What screening procedures/laboratory tests will you include (if available) in your assessment of Mrs. C., and why?

DIAGNOSIS (Identification of Problems/Needs) You have completed your assessment of Mrs. C. and your main findings include the following:

Mrs. C.'s pulse rate is 120 beats/minute and weak, blood pressure is 110/60 mm Hg, respiration rate is 20 breaths/minute and her temperature is 37 C. Her skin is pale and sweaty. Mrs. C. has constant abdominal pain, her uterus is tender on palpation, and the fetal heartbeat could not be heard. She has heavy vaginal bleeding containing some old clotted blood. Coagulopathy was not detected. 4. Based on these findings, what is Mrs. C.'s diagnosis, and why? 5. What laboratory test would be appropriate at this time? CARE PROVISION (Planning and Intervention) 6. Based on your diagnosis, what is your plan of care for Mrs. C., and why? EVALUATION Half an hour after admission, Mrs. C.'s condition has been stabilized, although she continues to bleed vaginally. Her cervix is found to be 3 cm dilated. Fetal heart sounds cannot be detected. Blood clotting test is normal.

7. Based on these findings, what is your continuing plan of care for Mrs. C., and why?

CASE STUDY 3.2: VAGINAL BLEEDING DURING LATER PREGNANCY ANSWER KEY CASE STUDY Mrs. C. who is 32 weeks pregnant, gravida three, has two healthy children. She has attended antenatal clinic regularly and all findings were within normal limits until her clinic visit 10 days ago. At that visit her blood pressure was noted to be 120/96 mm Hg; there were no other signs or symptoms of pregnancy-induced hypertension. Mrs. C. was counseled about danger signs and what to do if they occur and asked to return to the clinic in 2 weeks. She presents at the district hospital 2 days before her next clinic visit, accompanied by her mother-in-law, with vaginal bleeding, abdominal pain and a bad headache. ASSESSMENT (History, Physical Examination, Screening Procedures/Laboratory Tests) 1. What will you include in your initial assessment of Mrs. C., and why?

Mrs. C. and her mother-in-law should be greeted respectfully and with kindness.

They should be told what is going to be done and listened to carefully. In addition, their questions should be answered in a calm and reassuring manner.

A rapid assessment should be done to check for the following signs to determine if she is in shock and in need of emergency

treatment/resuscitation: rapid, weak pulse; systolic blood pressure less than 90 mm Hg; pallor; sweatiness or cold, clammy skin; rapid breathing; confusion. She should also be assessed to determine when vaginal bleeding started, the amount of blood lost, and whether the blood is bright and contains clots.

It will also be important to determine:

when abdominal pain started (e.g., at the same time as vaginal bleeding) and the nature of the pain

whether fetal movement has been felt since the onset of bleeding and pain

when headache started and whether there has been/is any visual disturbance (abruptio placentae can be associated with pregnancyinduced hypertension)

2. What particular aspects of Mrs. C.'s physical examination will help you make a diagnosis and identify her problems/needs, and why?

An abdominal examination should be done to establish the location and nature of pain, to feel the consistency of the uterus and check for guarding, and to detect fetal movement (a tense/tender uterus and decreased fetal movements are signs of abruptio placentae). Palpation should be kept to a minimum, however, to avoid exacerbating the symptoms.

An attempt should be made to detect fetal heart sounds, which may be absent with an abruption.

3. What screening procedures/laboratory tests will you include (if available) in your assessment of Mrs. C., and why?

No laboratory tests are required to make a diagnosis. However, an ultrasound scan may be performed if possible to locate placenta if placenta previa is suspected.

DIAGNOSIS (Identification of Problems/Needs) You have completed your assessment of Mrs. C. and your main findings include the following: Mrs. C.'s pulse rate is 120 beats/minute and weak, blood pressure is 110/60 mm Hg, respiration rate is 20 breaths/minute and her temperature is 37 C. Her skin is pale and sweaty. Mrs. C. has constant abdominal pain, her uterus is tender on palpation, and the fetal heartbeat could not be heard. She has heavy vaginal bleeding containing some old clotted blood. Coagulopathy was not detected. 4. Based on these findings, what is Mrs. C.'s diagnosis, and why?

Mrs. C.'s signs and symptoms (e.g., signs of shock, constant abdominal pain, uterine tenderness, vaginal bleeding, and absent fetal heart sounds) are consistent with abruptio placentae.

5. What laboratory tests would be appropriate at this time?

A bedside clotting test should be performed to detect or rule out coagulopathy (coagulopathy can be triggered by abruptio placentae).

CARE PROVISION (Planning and Intervention) 6. Based on your diagnosis, what is your plan of care for Mrs. C., and why?

Mrs. C. should be treated for shock immediately:

Position her on her side.

Ensure that her airway is open.

Give her oxygen at 68 L/minute by mask or cannula.

Keep her warm.

Elevate her legs.

Monitor her pulse, blood pressure, respiration and temperature.

Start an IV using a large bore needle for rapid infusion of fluids (1 L of normal saline or Ringer's lactate in 1520 minutes).

Monitor her intake and output (an indwelling catheter should be inserted to monitor urinary output).

Blood should be drawn for hemoglobin and cross-matching and blood for transfusion should be made available as soon as possible.

Arrangements should be made for childbirth as soon as possible.

The steps taken to manage the complication should be explained to Mrs. C. and her mother-in-law. Provide emotional support and reassurance, and answer any questions and concerns.

EVALUATION Half an hour after admission, Mrs. C.'s condition has been stabilized, although she continues to bleed vaginally. Her cervix is found to be 3 cm dilated. Fetal heart sounds cannot be detected. Blood clotting test is normal. 7. Based on these findings, what is your continuing plan of care for Mrs. C., and why?

Since vaginal delivery is not imminent, arrangements should be made to deliver Mrs. C. by emergency cesarean section. Blood loss should be replaced with blood transfusion, although the availability of blood for transfusion should not delay surgery. The nature of the procedure and the risks involved should be explained to Mrs. C. and her mother-in-law and continuing emotional support and reassurance should be provided. In particular, they should be prepared for the inevitability of a stillbirth.

Vigilant observation of Mrs. C.'s condition (vital signs, uterine involution, lochia) should be provided after childbirth, since there is a high risk of postpartum hemorrhage in women with abruptio placentae. In addition, Mrs. C. should be encouraged to see and hold her baby to facilitate grieving, and she and her family should be allowed to prepare the baby for its funeral, if they wish. Before discharge from hospital, possible preventive measures for the future should be discussed with Mrs. C. and her partner or, if she wishes, another family member.