Valvular heart disease is the most common cardiac problem complicating pregnancy, and pregnancy in most women with heart disease has a favourable maternal and fetal outcome. With the exception of patients with Eisenmenger syndrome, pulmonary vascular obstructive disease, and Marfan syndrome with aortopathy, maternal death during pregnancy in women with heart disease is rare. However, pregnant women with heart disease do remain at risk for other complications including heart failure, arrhythmia, and stroke. Women with congenital heart disease now comprise the majority of pregnant women with heart disease seen at referral centres. The next largest group includes women with rheumatic heart disease. Peripartum cardiomyopathy, though infrequent, will be discussed in view of its unique relation to pregnancy. Two groups of conditions not discussed further are coronary artery disease which is infrequently encountered, and isolated mitral valve prolapse, which generally has an excellent outcome. Hormonally mediated increases in blood volume, red cell mass, and heart rate result in a major increase in cardiac output during pregnancy; cardiac output peaks during the second trimester, and remains constant until term. Gestational hormones, circulating prostaglandins, and the low resistance vascular bed in the placenta result in concomitant decreases in peripheral vascular resistance and blood pressure. During labour and delivery, pain and uterine contractions result in additional increases in cardiac output and blood pressure. Immediately following delivery, relief of caval compression and autotransfusion from the emptied and contracted uterus produce a further increase in cardiac output. Most haemodynamic changes of pregnancy resolve by two weeks postpartum.

Poisoning refers to the development of dose-related adverse effects following exposure to drugs, chemicals, or other xenobiotics. To paraphrase Paracelsus, the dose creates the poison. Although most poisons have predictable dose-related effects, individual responses to a given dose may vary due to inhibition in the presence of other xenobiotics, genetic polymorphism, enzymatic induction, or acquired tolerance. Poisoning may be local (e.g. lungs, skin, eyes) or systemic depending on the route of exposure, the physical and chemical properties of the poison, and its mechanism of action. The reversibility and severity of poisoning also depend on the functional reserve of the target organ or individual which is influenced by preexisting disease and age. The history should include the route, duration, time, and circumstances (surrounding events, location, and intent) of exposure; the amount and name of each chemical, drug, or ingredient involved; the severity of symptoms, time of onset, nature of symptoms; the time and type of first-aid measures given; and the medical and psychiatric history. In most cases, the patient is unaware of exposure, confused, comatose, or unable or unwilling to admit to one. Suspicious circumstances include unexplained sudden disease in a previously healthy person or a group of healthy people; a history of psychiatric problems (especially depression); current changes in health, social relationships, economic status, or the onset of disease during work with chemicals or after ingestion of drink (especially ethanol), food, or medications. When patients become sick soon after arriving from a foreign country or being arrested for criminal activity, “body packing” or “body stuffing” (ingesting or concealing illicit drugs in a body cavity) should be suspected. Relevant information may be available from friends, paramedics, family, police, pharmacists, physicians, and employers, who should be queried regarding the patient’s, behavioral changes, habits, hobbies, available medications, and antecedent events. Patients have to be asked explicitly concerning their prescribed drugs and recreational medication use. Drugs previously considered “illicit” such as cannabinoids are now legal in many places and prescribed for therapeutic purposes. A search of belongings, clothes, and places of discovery may unveil a suicide note or a container of chemicals or drugs. Without an apparent history in a patient clinically suspected to be poisoned, all drugs available anywhere in the patient’s home or belongings should be considered as possible agents, including drugs for pets. The label on chemical products or the imprint code on drugs may be used to identify the potential toxicity of a suspected poison by consulting the manufacturer, a reference text, a computerized database, or a regional poison information center (800-222-1222). However, poisoning can mimic other illnesses, the correct diagnosis can usually be established by the history, physical examination, routine and toxicologic laboratory evaluations, and characteristic clinical course.

The critical feature that distinguishes the anemias discussed in this article is the presence of an inappropriately low reticulocyte count for the degree of anemia. This is consistent with nutritional deficiencies, decreased erythropoietin levels, aplastic anemia, or inherited bone marrow failure syndromes. In addition, bone marrow replacement by a benign or malignant process, including those associated with ineffective erythropoiesis (eg, congenital dyserythropoietic anemias), comprise the differential diagnosis. Anemia causes increased morbidity and mortality in pediatric population; the absolute reticulocyte count (ARC) can be calculated by multiplying the percent reticulocytes by the RBC count/L. In a patient with anemia, ARC values within the “normal range” (generally 50-100 × 109/L) indicate an inappropriate response and suggest that there is an underlying red cell production issue due to intrinsic or extrinsic factors, or a combination of the two. The mean corpuscular volume (MCV) is another valuable red cell index that narrows the differential diagnosis of anemia due to diminished production. It is critical, however, to check age-specific normal values for MCV and to recognize that certain diseases can present with low, normal, and/or high MCVs. Finally, the red cell distribution width (RDW) assists in differentiating whether the anemia is likely due to a mixed process (wide RDW) or from a single cause (normal RDW). However, the management of anemia depends on the etiology. Early diagnosis and prompt treatment improve the quality of life of patients.

Systemic Lupus Erythematosus(SLE) is a multisystem autoimmune disease with variable presentations. A proposed mechanism for the etiology of SLE involves the development of autoantibodies that result from a defect in apoptosis. The specific defect involves the “find-me” (adenosine triphosphate [ATP]/uridine triphosphate [UTP]) or “eat-me” (phosphatidylserine) signals activated upon release of red cell nuclei. In the absence of apoptosis, the nuclei break down, causing inflammation and contributing to the development of autoimmunity. Many signs and symptoms of SLE are caused by either circulating immune complexes or direct effects of antibodies on cells. A genetic predisposition for SLE exists, and the concordance rate in monozygotic twins is between 25% and 70%. If a mother has SLE, her daughter’s risk of developing the disease is 1:40, and her son’s risk is 1:250. The course of SLE consists of intermittent remissions punctuated by disease flares, and organ damage often progresses over time. Pericarditis is the most frequent cardiac manifestation; it can be documented by ECG, auscultation of a friction rub, or evidence of pericardial effusion. It usually responds to anti-inflammatory therapy and infrequently leads to tamponade. More serious cardiac manifestations are myocarditis and fibrinous endocarditis of Libman-Sacks. The endocardial involvement can lead to valvular insufficiencies, most commonly of the mitral or aortic valves, or embolic events. It has not been proven that glucocorticoid or other immunosuppressive therapies improve lupus myocarditis or endocarditis. Still, it is usual practice to administer a trial of high-dose steroids and appropriate supportive treatment for heart failure, arrhythmia, or embolic events. As discussed above, patients with SLE are at increased risk for myocardial infarction, usually due to accelerated atherosclerosis, which probably results from immune attack, chronic inflammation, and chronic oxidative damage to arteries.