حلوان, القاهرة, مصر النشرة الجوية
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¤ 5–10% of cholecystectomies
¤ More fulminant than calculous cholecystitis; may present w/ gangrene, perforation, & empyema.
¤ Risk factors: sepsis, ICU, TPN, immunosuppression, major trauma,
burns, diabetes, infections, mechanical ventilation, opiates, CHD & CABG, prolonged fasting, childbirth, nonbiliary surgery, & AIDS rarely seen in systemic vasculitides due to ischemic injury to gall bladder.
¤ Insidious presentation in already critically ill pts.
¤ Male predominance (80%)
Signs & Symptoms:
¤ Clinical presentation variable, depending on predisposing conditions
¤ RUQ pain absent in 75% of cases
¤ Fever or hyperamylasemia may be only clue
¤ Unexplained sepsis w/ few early localizing signs.
¤ Half of patients already have experienced complication: gangrene,
¤ RUQ pain, fever, & positive Murphy sign seen in minority.
¤ Leukocytosis w/ left shift in 70–85%
¤ Hyperamylasemia common
¤ Abnormal aminotransferases, hyperbilirubinemia, mild increase in serum alkaline phosphatase more common in acalculous than calculous cholecystitis.
¤ Plain x-ray: exclusion of a perforated viscus, bowel ischemia, or renal stones
¤ US: absence of gallstones, thickened gallbladder wall
° (>5 mm) w/ pericholecystic fluid, failure to visualize
° gallbladder, perforation w/ abscess, emphysematous cholecystitis; sensitivity of 36–96%; high false-negative rate.
° CT: thickened gallbladder wall (>4 mm) in absence of ascites or hypoalbuminemia, pericholecystic fluid, intramural gas, or sloughed mucosa; superior to US w/ sensitivity of 50–100%.
¤ Radionuclide cholescintigraphy (HIDA) scan: failure to opacify gallbladder; sensitivity almost 100%; false-positive rate of up to 40% in which gallbladder not visualized in spite of nonobstructed cystic
duct seen in severe liver disease, prolonged fasting, biliary sphincterotomy, hyperbilirubinemia; important not to allow test to delay treatment in very ill pts.
¤ Calculous cholecystitis, peptic ulceration, acute pancreatitis, rightsided pyelonephritis, hepatic or subphrenic abscess.
What to Do First
¤ CT: best test to exclude other pathology
¤ If suspect biliary sepsis, radionuclide study first; otherwise, CT first
¤ Blood cultures, IV broad-spectrum antibiotics
¤ Early recognition & intervention required due to rapid progression to gangrene & perforation.
¤ Cholecystectomy; both open & laparoscopic
¤ If evidence of perforation, then open cholecystectomy urgently; inflammatory mass may preclude successful laparoscopy.
¤ US-guided percutaneous cholecystostomy may be first choice in critically ill pts; success rate 90%; no surgery necessary if postdrainage
cholangiogram normal; catheter usually removed 6–8 wk.
¤ Transpapillary endoscopic drainage of gallbladder may be done when pt too sick for surgery & unsuitable for percutaneous drainage(massive ascites or coagulopathy).
¤ Routine post op. follow-up
complications and prognosis:
¤ <10% mortality in community-acquired cases.
¤ Up to 90% in critically ill pts.
What is bacterial meningitis?
Meningitis is an infection of the membranes (meninges) that protect the spinal cord and brain. When the membranes become infected, they swell and press on the spinal cord or brain. This can cause life-threatening problems. Meningitis symptoms strike suddenly and worsen quickly.
¤ Increased risk with exposure to meningococcal meningitis or travel
to meningitis belt (sub-Saharan Africa), but most cases sporadic.
¤ Increased incidence with extremes of age, head trauma, immuno-suppression.
What are the causes of bacterial meningitis?
Several different bacteria can cause meningitis:
What are the symptoms of bacterial meningitis?
Painful, stiff neck with limited range of motion.
Feeling confused or sleepy.
Bruising easily all over the body.
A rash on the skin.
Sensitivity to light.
¤ Prodromal upper respiratory tract infection progresses to stiff neck,fever, headache, vomiting, lethargy, photophobia, rigors, weakness,
¤ Fever, nuchal rigidity, signs of cerebral dysfunction; 50% with Neisseria meningitidis meningitis have an erythematous, macular rash that progresses to petechiae or purpura.
¤ Cranial nerve palsies (III, VI, VII, VIII) in 10–20%
¤ Elderly may to have lethargy or obtundation without fever, +/-meningismus.
¤ Basic Blood Tests:
° Elevated WBC
¤ Specific Diagnostic Tests:
° Blood cultures are often positive
° Typical cerebrospinal fluid (CSF) in bacterial meningitis (normal): opening pressure >180 mm H2O (50–150); color turbid (clear); WBC >1000/mm3 with polymorphonuclear cell predominance (5); protein >100 mg/dL (15–45); glucose <40 mg/dL (40–80); CSF/blood glucose ratio <0.4 (>0.6); Gram stain of CSF
shows organisms in 60–90%
° Culture of CSF is positive in 70–85%; community-acquired acute bacterial meningitis caused by Streptococcus pneumoniae, Neisseria meningitidis, Listeria monocytogenes, Haemophilus
influenzae, Escherichia coli, group B streptococcus
° Antigen testing for specific pathogens appropriate when a purulent CSF specimen has a negative Gram stain and culture, sensitivity 80%
¤ Other Tests:
° Patients with evidence of ICP such as coma or papilledema or focal neurologic findings (seizures, cranial neuropathies) should have a noncontrast CT scan prior to lumbar puncture (LP); begin antibiotics before CT scan
¤ Bacteremia, sepsis, brain abscess, seizure disorder, aseptic meningitis (CSF WBC usually 100–1000/mm3, eventually with lymphocyte predominance), skull fracture, chronic meningitis, encephalitis,
migraine headache, rickettsial infection, drug reaction
What to Do First
¤ Medical emergency: do not delay appropriate antibiotic therapy
¤ Quick neurologic exam looking for focality or evidence of increased ICP.
¤ Blood culture × 2
¤ If increased ICP or focality, start empiric antibiotics based on patient’s age and circumstances and send for CT of head without contrast
¤ If CT nonfocal and safe for LP, proceed to lumbar puncture.
¤ If neurologic exam normal, LP and base therapy on STAT Gram stain of CSF
¤ If CSF consistent with bacterial meningitis and positive Gram stain, start specific antibiotics. If consistent with bacterial meningitis with a negative CSF Gram stain, start empiric antibiotics
¤ Rigorous supportive care
¤ Dexamethasone IV before antibiotics and q6h × 2 d for children >1 mo and consider for adults with increased ICP or coma
¤ If strongly suspect meningitis, start IV antibiotics as soon as blood cultures drawn
¤ Empiric antibiotics (1):
° Age 18–50: ceftriaxone or cefotaxime +/-vancomycin (2)
° >50 years: ampicillin + ceftriaxone or cefotaxime +/− vancomycin (2)
° Immunocompromised: vancomycin + ampicillin + cetazadime
° Skull fracture: ceftriaxone or cefotaxime +/− vancomycin (2)
° Head trauma, neurosurgery, CSF shunt: vancomycin + ceftazadime
¤ Positive CSF Gram stain in community-acquired meningitis (1):
° Gram-positive cocci: ceftriaxone or cefotaxime + vancomycin (1)
° Gram-positive rods: ampicillin or penicillin G +/− gentamicin
° Gram-negative rod: ceftriaxone or cefotaxime
(1) Modify antibiotics once organism and its susceptibility are known; organism must be fully sensitive to antibiotic used.
(2) If prevalence of third-generation cephalosporin-intermediate + resistant S. pneumoniae exceeds 5%, add vancomycin until organism proved susceptible; if intermediate or resistant to cephalosporins, continue vancomycin and ceftriaxone or cefotaxime for possible synergy; if penicillin-susceptible, narrow to penicillin G; if penicillin-non-susceptible. and cephalosporin-susceptible, narrow to third-generation cephalosporin
¤ If dexamethasone used with vancomycin, consider adding rifampin
to increase vancomycin entry into CSF.
¤ Look for contiguous foci (sinusitis, mastoiditis, otitis media) or distant infection (endocarditis, pneumonia) with S pneumoniae
¤ Narrow coverage as culture results and susceptibility data allow
¤ If patient on adjunctive corticosteroids and not improving as expected, or if pneumococcal isolate, repeat LP 36–48 hours after starting antibiotics to document CSF sterility.
¤ Treat close contacts of patients with N meningitidis to eradicate carriage. If not treated with a third-generation cephalosporin, the patient should receive chemoprophylaxis as well.
complications and prognosis:
¤ Seizures, coma, sensorineural hearing loss, cranial nerve palsies, obstructive hydrocephalus, subdural effusions, CSF fistula (especially likely with recurrent meningitis), syndrome of inappropriate
¤ Consider placing ICP monitoring device
¤ ICP >15–20, elevate head to 30 degrees, hyperventilate adults
¤ Average case fatality: 5–25%
¤ N meningitidis: 3–13%
¤ S pneumoniae: 19–26%
¤ L monocytogenes: 15–29%
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¤ Enlargement of hands and feet
¤ Prognathism and loose teeth
¤ Increased sweating
¤ Sleep apnea and snoring
¤ Diabetes mellitus
¤ Coarsening change in facial appearance
¤ Frontal bossing
¤ Carpal tunnel syndrome
¤ Amenorrhea or oligoamenorrhea
¤ Family history of pituitary tumor
¤ Excessive linear growth (in children).
Signs & Symptoms:
¤ Skin tags
¤ Decreased libido
¤ Visual field cut
¤ Galactorrhea in some women.
¤ Basic blood studies:
° Insulin-like growth factor-I (IGF-I) single best test
° growth hormone (GH) 1 h after 75-g glucose load: <5 ng/dL in normals
¤ Ancillary blood tests:
° LH, FSH, prolactin, free T4, TSH
° GH-releasing hormone
° Fasting serum glucose, HgA1c
¤ MRI of the pituitary to determine if there is pituitary mass.
¤ GH-secreting pituitary tumor
¤ GH- and prolactin-secreting pituitary tumor
¤ GH- or GHRH-secreting neuroendocrine tumor (e.g., islet cell tumor of the pancreas).
¤ Acromegaloidism: acromegalic facies in patient with severe insulin resistance.
What to Do First:
¤ Assess size and resectability of tumor
¤ Surgical resection of tumor (usually transsphenoidal), esp. if there is visual field cut.
¤ Medical therapy:
° Somatostatin analog (octreotide or long-acting octreotide) given parenterally; can normalize serum IGF-I and GH; some tumor shrinkage
¤ Dopamine agonists (bromocriptine or cabergoline): may lower IGF-I and GH in some cases; often require high doses
¤ GH antagonists (pegvisomant) : very effective at lowering serum IGF-I; increases serum GH. Follow LFTs.
¤ Radiation therapy if surgery and medical therapy fail; may take up to 10 y to normalize serum IGF-I and GH; often causes hypopituitarism.
¤ Observation with repeated pituitary MRI to determine if tumor is growing
¤ Normalize serum IGF-I level
¤ Normalize GH response to glucose load
¤ Diminish size of pituitary tumor
¤ Maintain normal pituitary function
¤ Cessation of galactorrhea
¤ Restoration of libido and potency.
Side Effects & Contraindications:
¤ Surgery and radiation: hypopituitarism
¤ Octreotide: gallstones and gastric upset
¤ Bromocriptine and cabergoline: gastric upset, nasal stuffiness,orthostatic hypotension with initial doses.
¤ Serum IGF-I postoperatively or 2 wks after changing dose of medicine
¤ Repeat pituitary MRI after 3–6 mo to assess pituitary growth.
complications and prognosis:
¤ Pituitary apoplexy (in patients with macroadenomas):
° Presents as very severe headache, altered consciousness, coma
° Requires emergent surgical intervention and resection of tumor
¤ Visual field changes signify tumor growth
¤ Patients require lifelong observation
¤ Increased risk of colonic polyps and perhaps colon cancer
¤ Increased risk of early mortality (cardiac) if not cured (normal IGF-I levels).