Post Traumatic Stress Disorder

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What are the signs?

The symptoms of PTSD usually begin within 3 months of the traumatic event. However, sometimes they surface many years later. The duration of PTSD, and the strength of the symptoms, vary. For some people, recovery may be achieved in 6 months; for others, it may take much longer.

There are three categories of symptoms. The first involves re-experiencing the event. This is the main characteristic of PTSD and it can happen in different ways. Most commonly the person has powerful, recurrent memories of the event, or recur-rent nightmares or flashbacks in which they re-live their distressing experience. The anniversary of the triggering event, or situations which remind them of it, can also cause extreme discomfort. Avoidance and emotional numbing are the second category of symptoms. The first occurs when people with PTSD avoid encountering scenarios which may remind them of the trauma. Emotional numbing generally begins very soon after the event. A person with PTSD may withdraw from friends and family, they may lose interest in activities they previously enjoyed and have difficulty feeling emotions, especially those associated with intimacy. Feelings of extreme guilt are also common.

In rare cases, a person may enter dissociative states, lasting anywhere from a few minutes to several days, during which they believe they are re-living the episode, and behave as if it is happening all over again. The third category of symptoms involves changes in sleeping patterns and increased alertness. Insomnia is common and some people with PTSD have difficulty concentrating and finishing tasks. Increased aggression can also result.

Section XI/Chapter 119/ACID-BASE DISORDERS from Cecil Medicine

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Thus, respiratory acidosis is nearly always a consequence of decreased pulmonary ventilation from lung or central nervous system (CNS) disease rather than only increased production of CO₂. Respiratory alkalosis develops from hyperventilation rather than decreased CO₂production. In either case, when the elimination rate of CO₂ (the product of    a × Pco₂) again equals CO₂ production, a new steady state will prevail with no net carbonic acid retention or loss.

In metabolic disorders, if metabolic production of acid exceeds elimination, a state of metabolic acidosis exists, whereas if elimination exceeds production, metabolic alkalosis will develop. In the case of metabolic acidosis, production could exceed excretion via a marked excess in the production rate, as might be seen with diabetic ketoacidosis (DKA) or lactic acidosis, or it could develop even with a normal rate of metabolic acid production if the kidney were unable to eliminate acid normally, as in kidney failure.

MD Consult: Marx: Rosen's Emergency Medicine

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CAUSES OF HYPERKALEMIA

Pseudohyperkalemia    Hemolysis of sample    Thrombocytosis    Leukocytosis    Laboratory error    Increased potassium intake and absorption    Potassium supplements (oral and parenteral)    Dietary (salt substitutes)    Stored blood    Potassium-containing medications    Impaired renal excretion    Acute renal failure    Chronic renal failure    Tubular defect in potassium secretion    Renal allograft    Analgesic nephropathy    Sickle cell disease    Obstructive uropathy    Interstitial nephritis    Chronic pyelonephritis    Potassium-sparing diuretics    Miscellaneous (lead, systemic lupus erythematosus, pseudohypoaldosteronism)    Hypoaldosteronism    Primary (Addison's disease)    Secondary    Hyporeninemic hypoaldosteronism (renal tubular acidosis type 4)    Congenital adrenal hyperplasia    Drug-induced    Nonsteroidal anti-inflammatory drugs    Angiotensin-converting enzyme    Heparin    Cyclosporine    Transcellular shifts    Acidosis    Hypertonicity    Insulin deficiency    Drugs    Beta-blockers    Digitalis toxicity    Succinylcholine    Exercise    Hyperkalemic periodic paralysis    Cellular injury    Rhabdomyolysis    Severe intravascular hemolysis    Acute tumor lysis syndrome    Burns and crush injuries When faced with a report of a high serum K+ level, the emergency physician should first consider the possibility of laboratory error. Hemolysis during phlebotomy, as can occur when blood is obtained with a small needle or sampled in a high-vacuum tube, releases K+ into the sample and causes a spuriously high K+ measurement. Laboratory technicians usually note the presence of pink serum, indicating hemolysis. Pseudohyperkalemia can also occur when K+ is released from platelets in patients with severe thrombocytosis or from leukocytes in patients with extreme leukocytosis.[18] Hyperkalemia rarely results from increased K+ intake. This is more common when K+ supplements are inadvertently taken by patients with renal insufficiency or in those taking a K+-sparing diuretic or an angiotensin-converting enzyme inhibitor.[18] Parenteral medications such as penicillin and carbenicillin, as well as transfused blood, also contain significant amounts of K+ and can precipitate hyperkalemia. Renal insufficiency (i.e., decreased GFR), defects in tubular K+ secretion, or hypoaldosteronism can cause hyperkalemia. As GFR decreases to approximately 5 to 15 mL/min, excretion of the normal daily K+ load is impaired. Defects in tubular K+ excretion are associated with a number of conditions. Hypoaldosteronism may be the result of causes as varied as RTA type 4, Addison's disease, nonsteroidal anti-inflammatory drugs, and angiotensin-converting enzyme inhibitors. Transcellular K+ shifts (e.g., acute acidosis, beta-receptor antagonism) are another major cause of hyperkalemia. Periodic paralysis is an inherited disorder characterized by hyperkalemia caused by cellular efflux of K+ associated with stressors such as exercise, infection, and diet. Drugs may also be the cause of transcellular K+ shifts. Digitalis poisons the Na+-K+ ATPase pump, with resultant hyperkalemia in severe cases. Succinylcholine causes transient K+ efflux because of depolarization of the muscle cell membrane. High-dose trimethoprim-sulfamethoxazole has also been implicated in hyperkalemia, especially with concomitant renal insufficiency.[19,20] Life-threatening hyperkalemia may result when large amounts of K+ are released from damaged cells. Rhabdomyolysis, tumor cell necrosis, and hemolysis are important causes.[15] Acute renal failure that may be associated with these conditions impairs K+ excretion, further exacerbating endogenous hyperkalemia. Clinical Features Cardiovascular and neurologic dysfunction is the primary manifestation of hyperkalemia.[18] Patients may have a variety of dysrhythmias, including second- and third-degree heart block, wide-complex tachycardia, ventricular fibrillation, and even asystole. The ECG can provide valuable clues to the presence of hyperkalemia. As K+ levels rise, peaked T waves are the first characteristic manifestation. Further rises are associated with progressive ECG changes, including loss of P waves and widening and slurring of the QRS complex. Eventually, the tracing assumes a sine wave appearance, followed by ventricular fibrillation or asystole. Concomitant alkalosis, hypernatremia, or hypercalcemia antagonizes the membrane effects of hyperkalemia and may delay or diminish the characteristic ECG findings. Neuromuscular signs and symptoms of hyperkalemia include muscle cramps, weakness, paralysis, paresthesias, tetany, and focal neurologic deficits, but these are rarely specific enough to suggest the diagnosis in themselves.[15,16] Management The treatment of hyperkalemia includes cardiovascular monitoring, administration of calcium chloride or gluconate to treat hemodynamic instability, initiation of measures to lower serum [K+], and correction of the underlying cause. All patients with suggested hyperkalemia should be on a cardiac monitor, and attention should be paid to the morphology of the T waves and QRS complex. Peaked T waves, loss of P waves, slurring of the QRS, and second- or third-degree heart block all suggest hyperkalemia and are indications for prompt therapy. Treatment of the hyperkalemia is directed toward antagonism of the membrane effects of hyperkalemia, promotion of transcellular K+ shifts, and removal of K+ from the body. Calcium Chloride or Gluconate Immediate antagonism of K+ at the cardiac membrane is achieved with IV administration of calcium chloride or gluconate. This is indicated in patients with unstable dysrhythmia or hypotension. Several ampules of calcium (10 mL of 10% solution) may be required.[16,18] Because of the brief duration of action (approximately 20–40 minutes), other measures should also be instituted promptly.[18] Sodium Bicarbonate Sodium bicarbonate infusion promotes a shift of K+ into cells. One ampule (44 mEq) should be given by slow IV push over 5 to 15 minutes. The duration of action is approximately 2 hours. Sodium bicarbonate should be used with caution when hypertonicity, volume overload, or alkalosis poses a risk to the patient. Bicarbonate therapy is less efficacious than insulin or albuterol.[21,22] Glucose and Insulin Cellular uptake of K+ can also be induced with a regimen of IV glucose and insulin. Regular insulin (10–20 U) can be given by bolus infusion. Dextrose should be administered to euglycemic and diabetic patients with a blood glucose level below 250 mg/dL to prevent hypoglycemia. This combination lasts 4 to 6 hours.[18] Rapid infusion of hypertonic glucose solution may transiently exacerbate hyperkalemia by its osmotic effect on cells. Beta2-agonists The known effect of beta2-agonists to cause movement of K+ into cells can be harnessed to lower the serum K+ level acutely. Treatment with nebulized albuterol (5–20 mg) lowers the serum K+ level for at least 2 hours.[22,23] Exchange Resins Definitive treatment for hyperkalemia remains the removal of K+ from the body. Exchange resins (e.g., sodium polystyrene sulfonate [Kayexalate]) and hemodialysis are two such options. Given orally or rectally, each gram of Kayexalate can remove approximately 1.0 mEq of K+. An oral dose of 20 g of Kayexalate in a sorbitol produces effects in 1 to 2 hours. Rectal enemas of 50 g of Kayexalate, retained for 30 minutes, work in approximately 30 minutes. Kayexalate should be used with caution in patients with poor cardiovascular reserve because of the potential to exacerbate volume overload.

MD Consult: Mandell: Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases

lumbar puncture complications
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Numerous complications have been associated with performance of lumbar puncture,^[1,6-8] ranging from mild discomfort with insertion of the spinal needle to life-threatening conditions. The most common complication after lumbar puncture is headache, which is generally observed in 10% to 25% of patients, although may occur in up to 60% of patients; the headache is characteristically absent when the patient is recumbent and appears rapidly when the patient stands. The headache is believed to be secondary to low CSF pressure as a result of continued leakage of CSF at the site of the lumbar puncture. The risk of headache may be reduced by using smaller gauge needles (≤20 gauge) or by placing the patient in the prone position for several hours after the procedure, although it is unclear whether the latter maneuver is effective in reducing the likelihood of headache after lumbar puncture. A recommendation from the American Academy of Neurology supports the use of atraumatic (Sprotte or Pajunk) needles, rather than the standard (Quincke) needle, to reduce the risk of post–lumbar puncture headache.^[9] Reinsertion of the stylet before needle removal has also been shown to decrease the risk of headache.^[7] The headache usually resolves within hours to days after the procedure. Persistent headache can be treated by use of a "blood patch," in which some of the patient's own venous blood is injected outside the meninges at the site of the lumbar puncture; this procedure seals the site of CSF leakage.

Infection may occur after lumbar puncture, but the incidence of infection is low even in patients with concomitant bacteremia.^[1] Although there have been conflicting studies on the risk of subsequent meningitis in patients who are bacteremic at the time of lumbar puncture, the importance of performing a diagnostic lumbar puncture in the appropriate clinical setting greatly outweighs any minor risk that the procedure itself might induce meningitis in a bacteremic patient. Lumbar puncture should not be performed in patients with established local infection in the lumbar space (e.g., spinal epidural abscess, spinal subdural empyema, or superficial or deep paraspinal infection); in these cases, CSF analysis should be obtained under fluoroscopic guidance via high cervical or cisternal puncture.

Local bleeding is a more common complication after lumbar puncture^[1,6,8]; 20% of patients have a so-called traumatic tap.^[10] Bleeding may occur from inadvertent puncture of the venous plexuses located dorsally and ventrally to the spinal dura or secondary to injury to vessels that accompany the cauda equina. This local bleeding rarely does harm to the patient, although patients with coagulation disturbances or who are receiving anticoagulants may develop continued bleeding with the development of spinal subdural or epidural hematomas, which may compress the cauda equina and produce permanent neurologic injury.

The most feared complication after lumbar puncture is brain herniation, which may occur in a patient with an elevation of ICP.^[1,6-8] In patients who undergo lumbar puncture, there is normally a mild, transient reduction of lumbar CSF pressure that is rapidly communicated throughout the subarachnoid space. In patients with bacterial meningitis and suspected severe intracranial hypertension or impending herniation, a 22- or 25-gauge spinal needle should be used, with careful observation for several hours after removal of CSF; monitoring and treatment of increased ICP may need to be considered (see later). In patients who have an intracranial space-occupying lesion, particularly one located in the posterior fossa, there is already a relative pressure gradient (with downward displacement of the cerebrum and brain stem) that can be increased by lumbar puncture and precipitate brain herniation.

Certain patients should undergo neuroimaging studies (i.e., computed tomography [CT] or magnetic resonance imaging [MRI]) before lumbar puncture if there is a suspicion that their neurologic presentation may be secondary to an intracranial mass lesion with accompanying mass effect. These include patients with the following characteristics: immunocompromised state (HIV infection or AIDS, receiving immunosuppressive therapy, or after transplantation), history of CNS disease (mass lesion, stroke, or focal infection), new-onset seizure, abnormal level of consciousness, papilledema, or focal neurologic deficit (including dilated, nonreactive pupil; abnormalities of ocular motility; abnormal visual fields; gaze palsy; or arm or leg drift).^[1,11,12] It has been suggested, however, that a normal CT scan does not always mean performance of a lumbar puncture is safe. Certain clinical signs of impending herniation, such as a deteriorating level of consciousness (particularly a Glasgow Coma Scale score ≤11), brain stem signs (including pupillary changes, posturing, or irregular respirations), or a very recent seizure, may be predictive of patients in whom lumbar puncture should be delayed.^[13]

Acute Pancreatitis: Pancreatitis: Merck Manual Professional

Etiology
Biliary tract disease and alcoholism account for ≥ 80% of acute pancreatitis cases. The remaining 20% result from myriad causes (see Table 1: Pancreatitis: Some Causes of Acute Pancreatitis).

Table 1
Some Causes of Acute Pancreatitis Cause Example Drugs ACE inhibitors, asparaginase  , azathioprine  , 2´, 3´-dideoxyinosine, furosemide  , 6- mercaptopurine  , pentamidine , sulfa drugs, valproate  Infectious Coxsackie B virus, cytomegalovirus, mumps Inherited Multiple known gene mutations, including a small percentage of cystic fibrosis patients Mechanical/structural Gallstones, ERCP, trauma, pancreatic or periampullary cancer, choledochal cyst, sphincter of Oddi stenosis, pancreas divisum Metabolic Hypertriglyceridemia, hypercalcemia (including hyperparathyroidism), estrogen use associated with high lipid levels Toxins Alcohol, methanol Other Pregnancy, postrenal transplant, ischemia from hypotension or atheroembolism, tropical pancreatitis

Pregnancy, postrenal transplant, ischemia from hypotension or atheroembolism, tropical pancreatitis
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Menopause: Gynecology and Obstetrics: Merck Manual Professional

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Table 1 Effects of Oral Hormone Therapy on Yearly Incidence* of Selected Disorders in Postmenopausal Women Disorder Without Treatment With Treatment Combined Estrogen-Progestin Therapy Breast cancer 30 38 Colorectal cancer 16 10 Coronary artery disease† 30 37 Dementia 22 45 Ischemic stroke 21 29 Osteoporosis 15 10 Pulmonary embolism 16 34 Estrogen-Only Therapy Hip fractures 17 11 Ischemic stroke 32 44 *Per 10,000 women. †Number of coronary events such as nonfatal acute coronary syndrome and death due to coronary artery disease. Last full review/revision July 2007 by Susan L. Hendrix, DO Content last modified July 2007 Physiologic menopause is established when menses have been absent for 1 yr. In the US, average age of physiologic menopause is 51. Perimenopause refers to the years before (duration varies greatly) and the 1 yr after the last menses. Hormone therapy: For many women, risks of oral hormone therapy outweigh the benefits. Women who have a uterus and are given an estrogen must also be given a progestin.