Thursday, May 18, 2017

Introduction to Metabolic Alkalosis



A clinical state marked by decreased amounts of acid or increased amounts of base bicarbonate, metabolic alkalosis causes metabolic, respiratory, and renal responses, producing characteristic symptoms—most notably, hypoventilation. This condition always occurs secondary to an underlying cause. With early diagnosis and prompt treatment, the prognosis is good; however, untreated metabolic alkalosis may lead to coma and death.

Etiology
Metabolic alkalosis results from loss of acid, retention of base, or renal mechanisms associated with decreased serum levels of potassium and chloride.

Loss of acid
Causes of critical acid loss include vomiting, nasogastric tube drainage or lavage without adequate electrolyte replacement, fistulas, and the use of steroids and certain diuretics (furosemide, thiazides, and ethacrynic acid).
Hyperadrenocorticism is another cause of severe acid loss. Cushing’s disease, primary hyperaldosteronism, and Bartter’s syndrome, for example, all lead to retention of sodium and chloride and urinary loss of potassium and hydrogen.

Retention of base
Excessive retention of base can result from excessive intake of bicarbonate of soda or other antacids (usually for treatment of gastritis or peptic ulcer), excessive intake of absorbable alkali (as in milk-alkali syndrome), administration of excessive amounts of I.V. fluids with high concentrations of bicarbonate or lactate, or respiratory insufficiency—all of which cause chronic hypercapnia from high levels of plasma bicarbonate.

Mallory-Weiss syndrome



Mild to massive and usually painless bleeding due to a tear in the mucosa or submucosa of the cardia or lower esophagus characterizes Mallory-Weiss syndrome. Such a tear, usually singular and longitudinal, results from prolonged or forceful vomiting. About 60% of these tears involve the cardia; 15%, the terminal esophagus; and 25%, the region across the esophagogastric junction. Mallory-Weiss syndrome is most common in men older than age 40, especially alcoholics.

Causes
The direct cause of a tear in Mallory-Weiss syndrome is forceful or prolonged vomiting, probably when the upper esophageal sphincter fails to relax during vomiting. This lack of sphincter coordination is more common after excessive intake of alcohol. Other factors and conditions that may also increase intra-abdominal pressure and predispose to esophageal tearing include coughing, straining during bowel movements, trauma, seizures, childbirth, hiatal hernia, esophagitis, gastritis, and atrophic gastric mucosa.

Signs and symptoms
Typically, Mallory-Weiss syndrome begins with the vomiting of blood or the passing of large amounts of blood rectally a few hours to several days after normal vomiting. This bleeding, which may be accompanied by epigastric or back pain, may range from mild to massive but is generally more profuse than in esophageal rupture.
In patients with Mallory-Weiss syndrome, the blood vessels are only partially severed, preventing retraction and closure of the lumen. Massive bleeding—most likely when the tear is on the gastric side, near the cardia—may quickly lead to fatal shock.

Ulcerative colitis - Special considerations



Patients with ulcerative colitis need special care and management. Following points are important to remember:.
  • Accurately record intake and output, particularly the frequency and volume of stools.
  • Watch for signs of dehydration and electrolyte imbalances, specifically signs of hypokalemia (muscle weakness, paresthesia) and hypernatremia (fever, tachycardia, flushed skin, dry tongue).
  • Monitor hemoglobin and hematocrit, and transfuse if necessary.
  • Provide good mouth care for the patient who is allowed nothing by mouth.
  • After each bowel movement, thoroughly clean the skin around the rectum.
  • Administer medication. Watch for adverse effects of prolonged corticosteroid therapy (moonface, hirsutism, edema, gastric irritation). Be aware that such therapy may mask infection.
  • If the patient needs total parenteral nutrition, change dressings, assess for inflammation at the insertion site, and check blood glucose every 6 hours.
  • Take precautionary measures if the patient is prone to bleeding. Watch closely for signs of complications, such as a perforated colon and peritonitis (fever, severe abdominal pain, abdominal rigidity and tenderness, and cool, clammy skin), and toxic megacolon (abdominal distention, decreased bowel sounds).
  • Prepare the patient for surgery, and provide teaching related to the care of an ileostomy. Consult the enterostomal therapy nurse for preoperative teaching and stoma marking. Provide a bowel preparation.

Wednesday, May 17, 2017

Brief Summary of Inguinal Hernia



Introduction
A hernia occurs when all or part of a viscus protrudes from a normal location in the body. Most hernias are protrusions of part of the abdominal viscus through the abdominal wall. Although many kinds of abdominal hernias are possible, inguinal hernias are most common.
With an inguinal hernia, the large or small intestine, omentum, or bladder protrudes into the inguinal canal. Hernias can be reducible, incarcerated, or strangulated.

Pathophysiology

In males, during the 7th month of gestation, the testes normally descend into the scrotum, preceded by the peritoneal sac. If the sac closes improperly, it leaves an opening through which the intestine can slip. In either sex, a hernia can result from weak abdominal muscles or increased intra-abdominal pressure. An inguinal hernia may be indirect or direct.

Indirect inguinal hernia
An indirect inguinal hernia, the more common hernia, results from weakness in the fascial margin of the internal inguinal ring. This type of hernia enters the inguinal canal through the internal inguinal ring and emerges through the external inguinal ring. The hernia extends down the inguinal canal into the scrotum or labia.
An indirect inguinal hernia may develop at any age, is three times more common in males, and is especially prevalent in infants younger than age 1.

Understanding Bone marrow Transplantation



In bone marrow transplantation, usually 500 to 700 ml of marrow is aspirated from the pelvic bones of a human leukocyte antigen (HLA)–compatible donor (allogeneic) or of the recipient himself during periods of complete remission (autologous). The aspirated marrow is filtered and then infused into the recipient in an attempt to repopulate the patient’s marrow with normal cells.
This procedure has effected long-term, healthy survivals in about half of the patients with severe aplastic anemia. Bone marrow transplantation may also be effective in treating patients with acute leukemia, certain immunodeficiency diseases, and solid-tumor cancers.
Because bone marrow transplantation carries serious risks, it requires strict adherence to infection protection techniques and strict aseptic technique. It also requires that a primary caregiver provide consistent care and continuous monitoring of the patient’s status.

Before bone marrow infusion
  • Explain to the patient that the success rate depends on the stage of the disease and on finding an HLA-identical sibling match.
  • After bone marrow aspiration is completed under local anesthetic, apply pressure dressings to the donor’s aspiration sites. Observe the sites for bleeding. Relieve pain with an analgesic and ice packs as needed.
  • Assess the patient’s understanding of bone marrow transplantation. If necessary, correct any misconceptions about the procedure and provide additional information. Prepare the patient to expect an extended facility stay. Explain that chemotherapy and, possibly, radiation therapy are necessary to remove cells that may cause the body to reject the transplant.
  • Various treatment protocols are used. For example, I.V. cyclophosphamide may be used with additional chemotherapeutic agents or total body irradiation to suppress the patient’s immune system and requires aggressive hydration to prevent hemorrhagic cystitis. Control nausea and vomiting with an antiemetic (such as ondansetron, prochlorperazine, or metoclopramide) as needed. Give allopurinol, as prescribed, to prevent hyperuricemia resulting from tumor breakdown products. Because alopecia is a common adverse effect of high-dose cyclophosphamide therapy, encourage the patient to choose a wig or scarf before treatment begins.
  • Total body irradiation (in one dose or several daily doses) follows chemotherapy, inducing total marrow aplasia. Warn the patient that cataracts, GI disturbances, and sterility are possible adverse effects.