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By L. Pranck. Nova Southeastern University.

Approximately 2 L or 25 mL per kg should be given during the first hour to restore blood volume purchase phenergan 25 mg mastercard, stabilize blood pressure order line phenergan, and reestablish urine flow order generic phenergan. Because serum potassium concentration does not accurately reflect total body potassium, replacement should be initiated early during treatment. If a nasogastric tube is in place, electrolyte losses due to gastric suctioning must also be considered. As acidemia resolves, buffered intracellular H is + exchanged for extracellular K, further lowering the serum potassium concentration. A sudden reduction in serum potassium concentration can cause flaccid paralysis, respiratory failure, and life-threatening cardiac arrhythmias. Initially, the concentration of phosphate is elevated, but levels may decrease to less than 1 mmol per L within 4 to 6 hours of starting insulin treatment. Persistent severe hypophosphatemia can cause neurologic disturbances, arthralgias, muscle weakness with respiratory impairment, rhabdomyolysis, and liver dysfunction [47]. No studies have demonstrated that replacement of phosphate affects the course or outcome from ketoacidosis [48,49]. The hazards of parenteral phosphate administration include hypomagnesemia, hypocalcemia, and metastatic calcification [50]. Neutralization is intuitively appealing, but fluid and electrolyte replacement alone will ameliorate the acidosis, and bicarbonate therapy may produce adverse effects. These include severe acute hypokalemia [56], late alkalosis due to paradoxical cerebrospinal fluid acidosis [57], a shift in the oxygen dissociation curve to the left that results in tissue hypoxia and lactic acidosis [58], and increased hepatic ketogenesis [53]. Even in these circumstances, bicarbonate can only “buy time” until metabolic treatment reverses the acidosis. For some patients, Mg stores may be depleted, and hypomagnesemia may rarely lead to cardiac arrest [63]. For adults, we recommend a bolus of 10 U of short-acting insulin followed by a continuous intravenous infusion starting at 5 to 10 U per hour. If for some reason a continuous infusion cannot be given, an initial intravenous bolus of 10 units of short-acting insulin followed by repeated subcutaneous or intramuscular short-acting insulin injections can be used. Regular (crystalline) insulin is typically used for intravenous infusions; semisynthetic rapid-acting insulins approved for intravenous administration offer no advantage by this route. The onset of action of intravenous regular insulin occurs within minutes; bolus doses peak within 30 minutes, and the duration of action is 2 to 3 hours. Their shorter duration of action may, however, require more frequent monitoring of blood glucose concentration. If the glucose concentration has not decreased by 50 to 75 mg/dL/h, the insulin infusion rate should be doubled. When the glucose concentration has fallen by more than 150 mg per dL, the infusion rate should be decreased by 50%, but it should never be stopped. The entire clinical picture must be assessed, and when the acidosis and hyperglycemia are resolving, the rise in ketones should be interpreted as a sign of improvement. Persistent hypotension should prompt consideration of fluid shifts, bleeding, severe acidosis, hypokalemia, arrhythmia, myocardial infarction, sepsis, and adrenal insufficiency. Patients with gastric ulcer, colitis, or hemorrhagic pancreatitis can bleed into the gut lumen or peritoneum. Physical examination and an inappropriately low hematocrit in the face of dehydration are clues to this complication. Patients with hypotension and increased central venous pressure should be evaluated for heart disease. Myocardial infarction is the most common finding, but other conditions such as cardiac tamponade and diastolic cardiac dysfunction can occur. Myocardial infarction is a common complication of long-standing diabetes, and its classic symptoms may be less obvious in the diabetic population. Pyelonephritis and pneumonia are common among such cases and must be treated appropriately when encountered. It is not uncommon for patients with type 1 diabetes to have other autoimmune diseases, and adrenal insufficiency should be considered among cases of ketoacidosis with refractory shock. Cerebral edema has been associated with very high mortality (24%) [74], but a recent retrospective analysis shows current mortality rates are less than 10% [75]. Greater baseline acidosis, higher potassium and urea concentrations, and large volumes of administered fluids are also risk factors for cerebral edema [77]. The exact mechanism of cerebral edema is unknown, but it may involve a combination of fluid shifts, thrombosis of intracerebral vessels, and effects on ion exchange mechanisms [61,78]. The most effective treatment for cerebral edema is probably mannitol [75,79], although hypertonic saline is being used with increasing frequency [75,80]. Unfortunately, even when diagnosed early, cerebral edema may cause permanent neurologic damage or death. Recurrent Diabetic Ketoacidosis If ketoacidosis reappears for a patient who has received adequate amounts of insulin, infection or a severe contra-insulin state (e. Because the duration of action of intravenous insulin is brief and these patients make no insulin, ketone production resumes and ketosis soon recurs [2]. The intravenous infusion of insulin should be continued for 2 to 3 hours after the first subcutaneous injection of intermediate-acting or long- acting insulin is given so that the subcutaneous insulin has time to appear in the bloodstream. After insulin is given, glucose is metabolized as well as excreted, and blood glucose concentrations may fall rapidly. The physician must be alert to the possibility of precipitous reductions in glycemia and frequent monitoring of blood glucose is recommended. When the blood glucose concentration falls to 200 mg per dL, a D5 containing intravenous fluid should be administered together with insulin [85]. Of note is the fact that, with the increasing prevalence of obesity and type 2 diabetes among children, a similar disorder is being reported for the pediatric population [89,90]. The syndrome can be the initial presentation of type 2 diabetes and, in the United States, may occur with disproportionate frequency among African American youth. Patients have sufficient insulin to inhibit ketone body formation but not enough to prevent hyperglucagonemia, glycogenolysis, and gluconeogenesis [91]. Their resistance to ketosis must therefore depend on limited availability of circulating free fatty acids [95]. It has been suggested that, among children with baseline normal renal function, extreme hyperglycemia may be precipitated by intake of large amounts of sugary drinks to compensate for urinary fluid losses [89]. The common result is that affected patients are unable to compensate for the hyperglycemia with an osmotic diuresis. Severe hyperglycemia itself can cause prerenal azotemia because glycosuria causes a hypotonic osmotic diuresis resulting in urinary loss of free water. A common history involves an elderly patient with impaired cognitive function due to cerebrovascular disease, dementia, or central nervous system–depressant medications. This impairment may involve either concurrent impairment of the normal thirst mechanism or an inability to respond to thirst due to speech or motor deficits.

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Venlafaxine buy cheap phenergan online, bupropion buy phenergan 25mg free shipping, and escitalopram have very little effect on decreasing blood pressure (no α receptor antagonism) and are considered acceptable choices for treatment of depression in the1 elderly discount phenergan 25mg visa. Amitriptyline is associated with a high risk for orthostasis in the elderly and should be avoided due to its adverse effect profile and risk for falls. Overview the antipsychotic drugs are used primarily to treat schizophrenia, but they are also effective in other psychotic and manic states. The use of antipsychotic medications involves a difficult trade-off between the benefit of alleviating psychotic symptoms and the risk of a wide variety of adverse effects. Schizophrenia Schizophrenia is a type of chronic psychosis characterized by delusions, hallucinations (often in the form of voices), and disturbances in thought. Schizophrenia has a strong genetic component and probably reflects some fundamental developmental and biochemical abnormality, possibly a dysfunction of the mesolimbic or mesocortical dopaminergic neuronal pathways. Antipsychotic Drugs the antipsychotic drugs are usually divided into first- and second-generation agents. The first-generation drugs are further classified as “low potency” or “high potency. First-generation antipsychotics the first-generation antipsychotic drugs (also called conventional) are competitive inhibitors at a variety of receptors, but their antipsychotic effects reflect competitive blockade of dopamine D receptors. The second-generation drugs owe their unique activity to blockade of both serotonin and dopamine receptors. The2 second-generation antipsychotics exhibit an efficacy that is equivalent to, and occasionally exceeds, that of the first- generation antipsychotic agents. Differences in therapeutic efficacy among the second-generation drugs have not been established, and individual patient response and comorbid conditions must often be used to guide drug selection. Refractory patients Approximately 10% to 20% of patients with schizophrenia have an insufficient response to first- and second- generation antipsychotics. However, its clinical use is limited to refractory patients because of serious adverse effects. Clozapine can produce bone marrow suppression, seizures, and cardiovascular side effects, such as orthostasis. The risk of severe agranulocytosis necessitates frequent monitoring of white blood cell counts. Dopamine antagonism All of the first-generation and most of the second-generation antipsychotic drugs block D dopamine receptors in the2 brain and the periphery (ure 11. Actions the clinical effects of antipsychotic drugs reflect a blockade at dopamine and/or serotonin receptors. However, many antipsychotic agents also block cholinergic, adrenergic, and histaminergic receptors (ure 11. It is unknown what role, if any, these actions have in alleviating the symptoms of psychosis. However, the undesirable adverse effects of antipsychotic drugs often result from pharmacological actions at these other receptors. Antipsychotic effects All antipsychotic drugs can reduce hallucinations and delusions associated with schizophrenia (known as “positive” symptoms) by blocking D receptors in the mesolimbic system of the brain. The “negative” symptoms, such as2 blunted affect, apathy, and impaired attention, as well as cognitive impairment, are not as responsive to therapy, particularly with the first-generation antipsychotics. Many second-generation agents, such as clozapine, can ameliorate the negative symptoms to some extent. Extrapyramidal effects Dystonias (sustained contraction of muscles leading to twisting, distorted postures), Parkinson-like symptoms, akathisia (motor restlessness), and tardive dyskinesia (involuntary movements, usually of the tongue, lips, neck, trunk, and limbs) can occur with both acute and chronic treatment. Blockade of dopamine receptors in the nigrostriatal pathway is believed to cause these unwanted movement symptoms. Antiemetic effects the antipsychotic drugs have antiemetic effects that are mediated by blocking D receptors of the chemoreceptor2 trigger zone of the medulla (see Chapter 40). These effects include blurred vision, dry mouth (the exception is clozapine, which increases salivation), confusion, and inhibition of gastrointestinal and urinary tract smooth muscle, leading to constipation and urinary retention. Other effects Blockade of α-adrenergic receptors causes orthostatic hypotension and light-headedness. The antipsychotics also alter temperature-regulating mechanisms and can produce poikilothermia (condition in which body temperature varies with the environment). In the pituitary, antipsychotics that block D receptors may cause an increase in2 prolactin release. Sedation occurs with those drugs that are potent antagonists of the H -histamine receptor,1 including chlorpromazine, olanzapine, quetiapine, and clozapine. Sexual dysfunction may also occur with the antipsychotics due to various receptor-binding characteristics. Weight gain is also a common adverse effect of antipsychotics and is more significant with the second-generation agents. Treatment of schizophrenia the antipsychotics are the only efficacious pharmacological treatment for schizophrenia. The first-generation antipsychotics are generally most effective in treating the positive symptoms of schizophrenia. Other uses the antipsychotic drugs can be used as tranquilizers to manage agitated and disruptive behavior secondary to other disorders. However, risperidone and haloperidol are also commonly prescribed for this tic disorder. Also, risperidone and aripiprazole are approved for the management of disruptive behavior and irritability secondary to autism. Many antipsychotic agents are approved for the management of the manic and mixed symptoms associated with bipolar disorder. Some antipsychotics (aripiprazole, brexpiprazole, and quetiapine) are used as adjunctive agents with antidepressants for treatment-refractory depression. Some metabolites are active and have been developed as pharmacological agents themselves (for example, paliperidone is the active metabolite of risperidone, and the antidepressant amoxapine is the active metabolite of loxapine). These formulations usually have a therapeutic duration of action of 2 to 4 weeks, with some having a duration of 6 to 12 weeks. Adverse effects Adverse effects of the antipsychotic drugs can occur in practically all patients and are significant in about 80% (ure 11. Extrapyramidal effects the inhibitory effects of dopaminergic neurons are normally balanced by the excitatory actions of cholinergic neurons in the striatum. Blocking dopamine receptors alters this balance, causing a relative excess of cholinergic influence, which results in extrapyramidal motor effects. The appearance of the movement disorders is generally time- and dose dependent, with dystonias occurring within a few hours to days of treatment, followed by akathisias occurring within days to weeks. Parkinson-like symptoms of bradykinesia, rigidity, and tremor usually occur within weeks to months of initiating treatment.

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Cerebrovascular disease in children is most frequently etiology associated with several conditions purchase 25 mg phenergan, many of which are genetic buy 25mg phenergan otc. In addition discount phenergan 25mg fast delivery, the brain of a child is immature and the common causes of ischemic and hemorrhagic strokes are summarized in Table 6. The most frequently has more plasticity than adult brain, so recovery and final reported risk factors for stroke in children include cardiac outcome are better in younger patients than adults. Vascular malformation • Congenital heart disease • Arteriovenous malformations • Rheumatic heart disease • Aneurysm • Infective endocarditis • Angiomas • Complication of cardiac surgery B. Miscellaneous 392 • Hypotension disorders, coagulation disorders, iron deficiency anemia, internal capsule, there is dense hemiplegia with facial nerve sickle cell disease, infection, Moyamoya vasculopathy, palsy of upper motor neuron type. Focal 80% of cases, are age-related, and differ significantly from signs may be absent in neonates or young infants, in whom adults. Embolic stroke secondary to congenital heart seizures may be the only manifestation of clinical stroke. Varicella has been identified as an manifestations of sinovenous thrombosis in children are important risk factor for childhood stroke and is reported to altered sensorium, headache and focal neurologic signs account for a significant proportion of ischemic strokes. Cervicocerebralarterial dissections have been increasingly Underlying risk factors including prothrombotic states recognized as a cause of stroke. Arterial dissections may occur may “predispose” the patient to thrombosis, while acute in internal carotid artery or vertebral artery. Hemorrhagic stroke Moyamoya disease is characterized by progressive the hemorrhage can be parenchymal or extracerebral. Onset stenosis and occlusion of the cerebral arteries at the circle of is apoplectic in hemorrhagic stroke with loss of consciousness Willis. Signs of raised intracranial pressure and mass small collateral vessels develops, creating the characteristic effect are usual. The possible underlying mechanism includes diagnostic evaluation thrombocytosis leading to hypercoagulable state and anemic hypoxia. The diagnostic evaluation in a patient with stroke is aimed Risk factors for cerebrovascular disease are outlined in at confirming the diagnosis of cerebrovascular disease, Table 6. The clinical features at presentation vary with age of the A patient presenting with stroke should be investigated patient, the type of stroke and extent of involvement. All patients coming with acute onset Embolism produces a rapidly evolving clinical picture, with neurological deficit should first undergo neuroimaging. There may be a prodromal period of days to weeks, and hemorrhage and rule out other diagnosis. Imaging of the arterial ischemic stroke This is the most common clinical type of stroke seen Table 6. It typically presents with acute onset of • Intracranial infections neurological deficit such as hemiparesis with or without • Cerebral tumors seizures. After confirming the existence of infarct or hemorrhage, After stabilizing the patient, a thorough search should one should investigate further to determine the etio- be made for the underlying cause responsible for the logy of stroke. All patients should have a chest x-ray, event and specific treatment should be instituted for the electrocardiogram and echocardiogram as underlying heart underlying etiology. Revascularization surgery should be disease is a very common cause of stroke in the pediatric considered in patient with Moyamoya disease to prevent population. Patients with unexplained stroke Prevention of recurrence should be screened for prothrombotic states. Signs of trauma and raised intracranial pressure its proper application may well determine ultimate motor should be looked for and appropriately managed. As soon as possible after admission, the child presentation it is essential to make the distinction between should have an evaluation of: hemorrhagic and ischemic stroke, since the former may • Ability to feed safely require neurosurgical intervention. Tissue plasminogen • Communication activator is the only approved treatment for acute ischemic • Positioning requirements stroke in adults. A comprehensive assessment of speech and language Anticoagulation should be considered in children with: should be made and speech therapist should be involved in • Confirmed extracranial arterial dissection associated the rehabilitation program. Recent developments the treatment for hemorrhagic stroke in children in childhood arterial ischaemic stroke. Cerebral venous sinus Treatments for vascular malformations include surgery, (sinovenous) thrombosis in children. Patients with sickle cell disease Diagnosis and management of pediatric arterial ischemic benefit from blood transfusion or exchange transfusion. The onset of floppiness in these infants is usually metabolism) and miscellaneous disorders. Floppy infant, Certain systemic disorders like septicemia, meningitis, often termed floppy infant syndrome, is not a disease encephalitis, bulbar poliomyelitis, acute transverse myelitis, but a clinical condition associated with a large number of acute severe malnutrition and hypokalemia can cause acute diseases and disorders. They usually present with floppiness, onset hypotonia; however these are usually not labeled as diminished motor activity and/or certain complications like floppy infant but are diagnosed according to the primary feeding difficulty and pneumonia. A list of such disorders based on published most common genetic disorders are Down and Prader- Table 6. Metabolic and other disorders as causes of • History of prenatal, intranatal, neonatal and postneonatal floppy infant are relatively uncommon. Some disorders like problem perinatal insult, Guillain-Barre syndrome, infant botulism • Weakness relatively less severe compared to the degree and certain inborn errors of metabolism can have acute of hypotonia and stormy presentation. However, the course is usually • Brisk tendon reflexes protracted and prolonged and hypotonia continues to • History of seizures remain as a predominant feature. A systematic approach through • Profound motor weakness proportional to the severity good history, thorough examination and etiology-oriented of hypotonia diagnostic investigation is necessary. In history, emphasis • Decreased or absent tendon reflexes should be given on bad obstetrical history, prenatal- • Relatively preserved cognitive function intranatal-neonatal stress, postneonatal problems, • No history of seizure. Genetic cause should be suspected in presence of: Neurological examination needs to be through with • History of bad obstetrical history special emphasis on tone, power, reflexes, sensation and • Consanguinity development. The most important areas in examination of • Positive family history a floppy infant are tone and power of muscles. Hypotonia in floppy infants is usually accompanied dehydration, acidosis, seizures, coma, respiratory abnor- by motor weakness that needs careful assessment to rule mality, organomegaly, rash and failure to thrive. Power in floppy infant is examined by: investigations • Observation of movement, spontaneous and on stimulation Etiology of floppy infant is diverse; there cannot be a set • Using the standard pull-push technique at joints giving of routine investigation for the condition. Investigations varying resistance (kinetic power) have to be guided by clinical suspicion based on • By trying to move a limb held static by the infant and history and clinical examination. Proximal weakness is more common in not always be possible to pin-point the etiology on clinical myopathies and muscular dystrophies, and distal weakness ground as several signs and symptom are shared by many is more common in peripheral neuropathies. Some such features are given in Table arrived at based on history and examinations, i. Imaging is often done to confirm any brain At the end of the examination, efforts should be made pathology if clinically suspected. Muscle biopsy with special staining is needed • Decreased fetal movement (myotubular myopathy, nemaline rod to arrive at the definitive diagnosis of myopathies.

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