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#62
30.03.2006, 10:01
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The EMT squad has just left your office, headed for the local community hospital with one of your patients in an ambulance. A short time ago, the 4-year and 11-month-old boy experienced a left-sided focal seizure in an examining room of the practice that progressed to a generalized tonic-clonic seizure. You were able to control the seizure with intravenous lorazepam, 0.1 mg/kg of body weight, while awaiting EMS. Now, you pause in the middle of an otherwise routine day of appointments to ask: What chain of events led to these tense moments?
Just over three weeks ago, this Caucasian boy, who has a notable history of cognitive developmental delay and reported penicillin allergy, was seen by one of your partners for right-sided acute otitis media (AOM). Despite the boy's speech delay, he is known in the practice to be able to communicate appropriately with his mother, and had complained of right-ear pain. Your partner, his regular pediatrician, started the patient on cefdinir (Omnicef). An uneventful three weeks passed. Then, today, the boy was brought in by his mother with a four-day history of fever (maximum recorded axillary temperature, 102°F) and discharge from the right ear, along with an upper respiratory tract infection. In your partner's absence, you saw the patient. He wasn't in discomfort and hadn't complained of earache at home. Other than the discharge, fever, and respiratory complaint, your exam was unremarkable. You prescribed ofloxacin otic drops (Floxin Otic) for possible perforated AOM and advised his mother to bring the boy back in 72 hours for a recheck. But the patient's mother returned just 10 minutes later, her son in her arms, agitated because he "wasn't making eye contact and was stiff with his jaws locked up". As she explains this, the seizure begins; you and your staff take action, and EMS is called. Deterioration on admission The story picks up on the pediatric ward of the community hospital, where the boy has been admitted. Blood, cerebrospinal fluid (CSF), and urine specimens are immediately sent for culture. The patient undergoes noncontrast cranial computed tomography; the radiologist interprets the scan as right-sided mastoiditis—"opacity of the right mastoid without gross evidence of bone destruction." Spinal tap reveals the following CSF values: cell count, 7/mm3 (with a differential count of 92% neutrophils and 8% lymphocytes); glucose, 65 mg/dL; and protein, 83 mg/dL. Complete blood count reveals a white blood cell count of 5.6 X 103 /μL (with a differential count of 23% segmented neutrophils, 47% band forms, 14% lymphocytes, and 16% monocytes); hemoglobin, 11.4 g/dL; and a platelet count of 214 X 103 /μL. Urinalysis parameters are within normal ranges. A blood chemistry panel shows a serum sodium level of 137 mmol/L; potassium, 2.9 mmol/L; chloride, 103 mmol/L; bicarbonate, 22 mmol/L; glucose, 172 mg/dL; blood urea nitrogen, 2 mg/dL; serum creatinine, 0.8 mg/dL; aspartate aminotransferase, 304 IU/L; alanine aminotransferase, 149 IU/L; serum alkaline phosphatase, 154 IU/L; total bilirubin, 2.5 mg/dl; total protein, 3.6 g/L; serum albumin, <2.0 g/L; serum ammonia, 43 μmol/L (reference rage, 11 to 35 μmol/L); and serum lactate dehydrogenase, 575 IU/L (reference range, 76 to 182 IU/L). The low serum albumin level is judged to likely reflect increased vascular permeability secondary to incipient septic shock. Because the boy is deteriorating clinically, he is transferred to the pediatric intensive care unit. Intravenous cefotaxime is started. With a prothrombin time of 22.2 sec (reference range, 10.2 to 12.3 sec) and an INR of 3.7, as well as an activated partial thromboplastin time of 40 sec (range, 24 to 35 sec), he is also given human activated protein C (drotrecogin [Xigris]) for disseminated intravascular coagulation, and vasopressors for hypotension associated with the septic shock. When preliminary results of blood and CSF cultures showed gram-positive cocci that evening, IV vancomycin is added to cover the usual suspect, Streptococcus pneumoniae. Based on the dictum that not every patient reads the book, the real "shock" comes afterward—but it's for you and the medical team. Within four and 14 hours, cultures of CSF and blood, respectively, grow β-hemolytic group A streptococcus (GAS)! Not a customary culprit GAS is the cause of a variety of common clinical illnesses, including tonsillopharyngitis, scarlet fever, cellulitis, cervical lymphadenitis, erysipelas, and otitis media. Although necrotizing fasciitis, osteomyelitis, sepsis and toxic shock syndrome are well recognized among invasive GAS infections, GAS-associated meningitis occurs but rarely, accounting, in various studies, for none to 3.2% of all bacterial meningitides and for 0.8% of all invasive GAS infections reported in the US between 1995 and 1999. GAS meningitis has been reported in all age groups, with disproportionately higher incidence in children. The prevalence of comorbid conditions is high among all age groups: In one report, 67% of patients had a concomitant or earlier neurosurgical condition. That report also noted the growth of variable M-type GAS with genotypic variability of speC and speA in strains isolated from different patients. Among adults, GAS meningitis is often preceded by otitis media or sinusitis. In one retrospective study, 80% of patients had an extrameningeal focus, predominantly in the ear, nose, throat, and upper respiratory tract.Similar to what was seen in your patient, an association between GAS meningitis and both OM and mastoiditis has been documented in several pediatric case reports and case series. Newborns, patients with a CSF leak, and those who have an immunosuppressive condition are the groups at high risk of GAS meningitis. Your patient was in none of these categories. GAS meningitis is a virulent disease, with a mortality of 10% to 12% and a high incidence of neurologic sequelae in children and adults. Mortality from GAS meningitis is comparable to mortality associated with Haemophilus influenzae and Neisseria meningitidis meningitis. Overall, the incidence of neurologic sequelae among children who have had GAS meningitis is 36% to 46%.(In fact, your patient had residual left-sided hemiparesis at discharge.) Timeline of subsequent events Clinical case definition of streptococcal TSS in a child The boy had a protracted hospital course, exhibiting clinical features of meningitis and septic shock. In addition, the clinical findings fulfill the definition of streptococcal toxic shock syndrome (TSS) . Notwithstanding what was seen in this case, TSS is rarely associated with meningitis in invasive GAS infection. The other unusual finding here was a low WBC count in CSF; a recent review of the international literature on GAS meningitis reported otherwise. Once the pathogen was confirmed, and in light of the TSS, the antimicrobial regimen was switched to a four-week course of ampicillin and clindamycin to treat the mastoiditis. (Note: The boy tolerated ampicillin well; the rash reported to your partner by his parents when the boy was an infant, and assumed to be penicillin allergy because it was coincidental to a course of amoxicillin was apparently of a different, unknown cause.) He was also given 2 g/kg of IV immune globulin for the TSS. After recovery from the acute illness, the patient was transferred to a children's hospital for neurorehabilitation. Before transfer, he underwent brainstem auditory evoked response testing which confirmed bilaterally normal hearing. A magnetic resonance imaging scan of the brain showed right-sided cerebral infarcts in the parieto-occipital areas. Drug of the hour: Clindamycin The efficacy of clindamycin in GAS infection is independent of the size of the inoculum or the stage of bacterial growth. Additionally, the drug suppresses both synthesis of bacterial toxin and release of penicillin-binding proteins that are involved in cell-wall synthesis and degradation. Clindamycin also has a longer post-antibiotic effect compared to that of β-lactam antibiotics. It enhances phagocytosis of GAS by inhibiting M-protein synthesis—observations that are based on animal and in vitro studies. It is also postulated that the effectiveness of clindamycin may be related to its ability to modulate host immune response. Because the minimum inhibitory concentration of penicillin has remained relatively unchanged for GAS isolates in the past eight decades, penicillin, 250,000 U/kg/day to a maximum of 24 million U every 24 hours, is recommended to attain a CSF level of 1 μg/mL. The usual empiric choice of a third-generation cephalosporin to cover more common bacteria that cause meningitis does suffice to treat GAS, although it is advisable to tailor therapy with antibiotics specific to GAS.3 (For a discussion of selecting antibiotics empirically, read What bug, which drug? Optimizing empiric antimicrobial therapy). A minute of your time, please! Except for residual, but improving, left hemiparesis, the patient's clinical course has been unremarkable since he was discharged from the children's hospital and returned to your practice. In accordance with recommendations made by the Centers for Disease Control and Prevention for invasive GAS disease among household contacts of index patients, no other of the boy's family members were screened, or offered chemoprophylaxis, for GAS. To sum up: GAS is rare in the era of antibiotics. Always take a few minutes, however—10, say?—to consider it as a cause of meningitis that is associated with recurrent otitis media and mastoiditis. 
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#64
20.04.2006, 10:22
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Being on call for the hospital's pediatric general medicine and infectious disease services has kept you busy this morning, admitting children with dehydration from gastroenteritis and initiating sepsis work-ups for febrile infants. And once again, your pager displays the emergency department number.
In the ED, the team reports that your next admission is a 6-month-old boy who has been vomiting. His name seems familiar.... That's it! About a month ago, you heard your colleagues discussing this child's case during an earlier admission—they were describing him as one who hadn't fared well in the game of "formula roulette." You don't know the details of how the formula had been changed, but you do remember that he was admitted then with vomiting, hyponatremia, and failure to thrive. You look at the chart for background and one notation is prominent: A diet history that was taken at the prior visit to the ED a month ago revealed that the first-time parents, having grown frustrated with their baby's persistent vomiting, decided to feed him with their own formula of 1:1 cow's milk and water. A few days afterward, he was admitted, rehydrated with intravenous fluids, and started on commercial ready-to-feed, iron-fortified, milk-based infant formula. The vomiting ceased by the third day after admission and the sodium level improved by discharge. His parents were given explicit instructions not to dilute the premixed formula. As you walk into the examining room, the young mother is playing with your babbling patient, who is nearly sitting independently (tripoding) and who appears to be the size of, roughly, a 2-month-old. The mother appears tired and is hunting through two of her bags for the baby's favorite toy; one bag appears to be a backpack containing heavy textbooks and the other is full of baby supplies, including the ready-to-feed formula. When, you ask, did the vomiting begin? And what has been done so far to try to stop it? The mother explains that the baby has been seen at several different clinics—at first because of health insurance problems, later because she and her husband saw no improvement in his vomiting and poor growth. The vomiting began at about 3 months of age, while the baby was being breastfed; various physicians noted that he was "growing slowly." The vomiting is always postprandial, she explains, involves food only, and is never forceful. It is also nonbilious and nonbloody. The child's pediatrician encouraged the mother to continue breastfeeding because there was no blood in the stool to support a milk-protein allergy. At-home empiric trials of ranitidine (Zantac) and metoclopramide (Reglan) were started for gastroesophageal reflux. The baby continued to vomit and was unable to keep down the medications. The parents decided to try a standard milk-based infant formula—in fact, they tried several brands. They returned to the clinic for the 4-month well-child visit with the baby still experiencing postprandial emesis and having poor weight gain. Formula for trouble? But the infant seemed to vomit even more when given a milk-based formula than when breastfed, so the pediatrician again entertained the idea of milk-protein allergy and switched the diet to, first, a soy-based formula and then to a protein hydrolysate-based formula. Plans were made for an outpatient upper gastrointestinal radiographic series and abdominal ultrasonography (US) to evaluate for reflux and anatomic abnormalities. Because vomiting persisted even with hydrolysate-based formula, the parents decided, on the recommendation of a family member, to try the ill-advised diluted cow's milk diet you read about earlier. A few days before the scheduled radiographic studies, the infant began vomiting after every meal and was taken to the ED. He had by then been taking the diluted cow's milk for five days. Once the baby was rehydrated and discharged, according to his mother, the vomiting restarted intermittently after about one week, and had become much worse in the past two days. She asserts that she has given him ready-to-feed formula only, three or four ounces every four hours, as well as homemade pureed baby food. She also comments that he seems more interested in eating food if it is salty, and that he tends to vomit less when table salt is added to each mouthful! Now, fill in the blanks! You file that curious observation away for a moment and proceed with a review of systems, which is otherwise negative except for a mild case of apparent atopic dermatitis that is not being treated. The patient has not had diarrhea or constipation. The usual stool pattern is one soft stool every one or two days since he has been given formula—as opposed to five or six stools a day when he was breastfed. He has not had fever, prior infection, polyuria, or polydipsia. The birth history is unremarkable. The baby was born at term by uncomplicated vaginal delivery. He was born in Ohio, where standard newborn screening includes a test for congenital adrenal hyperplasia; all tests on the screen were negative. The patient is not taking any medications at the moment. The only medications he has been given include occasional acetaminophen and the brief trials of ranitidine and metoclopramide. Immunizations are up to date. The family history is unremarkable, and specifically negative for childhood deaths, congenital anomalies, failure to thrive, and cardiac, thyroid, adrenal, and renal disease. He is the first child of a young married couple from Macedonia. The parents deny consanguinity. They are graduate students who plan to return to Macedonia after graduation in the next few months. On physical exam, the baby is alert, afebrile, and interactive and appears developmentally appropriate for the age of 6 or 7 months. He is, however, very small for his age. He is also hypertensive (blood pressure, 118/78 mm Hg). Heart rate is 146/min; respiratory rate, 30/min. Weight is 5.3 kg (well below the third percentile); he has gained only 240 g since discharge one month ago. Length is 63.5 cm (also at the third percentile) and head circumference is at the 25th percentile. The head is normocephalic, with a soft, open anterior fontanel. The pupils are equally round and reactive to light, with no eye abnormalities. Mucous membranes are moist without lesions. The neck is supple without palpable masses. The chest is clear to auscultation. The heart rhythm is regular, with normal heart sounds and without murmur. The abdomen is soft without organomegaly. The genital exam reveals a normal Tanner stage-I male with bilaterally descended testes and normal penile length. The neurologic exam reveals normal tone and no focal findings. Skin is without hyperpigmentation. A basic metabolic profile that was ordered on arrival in the ED is significant for a sodium level of 126 mmol/L; potassium (non-hemolyzed), 6.2 mmol/L; chloride, 91 mmol/L; and mild metabolic acidosis . A differential diagnosis as wide and as deep as the sea You pause to summarize what you've seen so far. Here is a 6-month-old male with several significant findings: * persistent vomiting * failure to thrive even with appropriate feeding * recurrence of hyponatremia * mild hyperkalemia * hypochloremia * hypertension. Also notable is that the child appears euvolemic on physical examination. The differential diagnosis of hyponatremia and failure to thrive with vomiting is extensive. Common causes include incorrect preparation or dilution of formula and vomiting brought on by gastroesophageal reflux, pyloric stenosis, difficulty swallowing, intestinal malrotation with obstruction, and central nervous system lesions characterized by elevated intracranial pressure. Even though the parents have not reported a history of diarrhea, your exhaustive initial differential includes diarrheal diseases that lead to hyponatremia and failure to thrive. These include infection (viral, bacterial, and parasitic) and malabsorption from cystic fibrosis, celiac disease, and a congenital deficiency of any of several enzymes involved in the digestion of carbohydrates and proteins. Less common causes of hyponatremia and failure to thrive include chronic liver disease (including glycogen storage disorders) and endocrine disorders such as hypothyroidism, diabetes mellitus (with pseudohyponatremia), and glucocorticoid or mineralocorticoid deficiency. In addition to adrenal hormone deficiencies, other renal salt-wasting conditions include nephritis, cystic disease, obstructive uropathy, use of a diuretic, renal tubular acidosis, and the syndrome of inappropriate antidiuretic hormone secretion (associated with tuberculosis, hypothyroidism, lung and CNS processes, and use of various medications).
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#65
20.04.2006, 15:12
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продолжение
One toe in the water
The first step in evaluating hyponatremia, you recall, is to assess possible causes of pseudohyponatremia associated with elevated plasma osmolality secondary to hyperglycemia, hyperproteinemia, and hyperlipidemia. The second step is to evaluate urine osmolality for water excess conditions, such as water intoxication of infancy (or, in an adult, psychogenic polydipsia); water excess is brought to light when urine osmolality <100 mOsm/kg of water. Third, if water excess is ruled out and a case of true hyponatremia is thereby confirmed, the patient's volume status is gauged by physical exam and the cause of sodium loss is determined to be renal or extrarenal. You review the laboratory studies from the first admission and note hyponatremia (122 mmol/L on admission, improving to 132 mmol/L at discharge) with hyperkalemia (6.6 mmol/L at admission, improved at discharge), mild metabolic acidosis, a normal sweat chloride test, normal random 17-hydroxyprogesterone level (which rules out 21-hydroxylase deficiency, the most common cause of congenital adrenal hyperplasia), and normal thyroid-stimulating hormone and free T4 values. An acute abdominal radiographic series and an upper-GI series with small-bowel follow-through were unremarkable. The possibility of a work-up for a glucocorticoid or mineralocorticoid deficiency had been discussed, but the patient had improved so rapidly with hydration and correction of the formula that it was decided to not pursue such an extensive laboratory investigation unless the problem recurred. Serial metabolic profiles obtained during this second admission have confirmed persistent hyponatremia, mild hyperkalemia, and hypochloremia. With the admission sodium deficit calculated to be 53 mmol,* the patient was hydrated using 5% dextrose in ½ normal saline over 36 hours for planned maximal correction of sodium by 0.5 mmol/h. You recall the mother's comment that the baby favors salty foods; this suggests salt craving. Urinalysis is unremarkable, with a urine specific gravity of 1.009. Fractional excretion of sodium (FENa)† is inappropriately high, at 1.48%. Urinary random electrolytes reveals an elevated sodium level of 70 mmol/L (normal, <25 mmol/L) and potassium level of 34.1 mmol/L. The ratio of urine osmolality (294) to serum osmolality (267) is inappropriate, given the hyponatremia. The combination of the elevated FENa and the random urine sodium level of 70 mmol/L suggests renal salt wasting. The lack of hyperpigmentation on your physical examination is inconsistent with a diagnosis of chronic primary glucocorticoid insufficiency, because an elevated adrenocorticotropic hormone (ACTH) level, in response to a low cortisol level, leads to hyperpigmentation because melanocyte stimulating hormone is produced as a byproduct of excess production of ACTH. You rule out glucocorticoid insufficiency with a normal ACTH level and a normal ACTH stimulation test, with an appropriate increase in cortisol from 6.3 to 25 μg/dL after one hour. At this point, the differential diagnosis of hyponatremia with failure to thrive, plus documented renal salt wasting despite normal renal function, includes mineralocorticoid deficiency or resistance to the action of aldosterone. Mineralocorticoid deficiency can be 1) a primary deficiency of aldosterone secondary to an abnormality of the adrenal glands or 2) a secondary aldosterone deficiency resulting from a hyporeninemic condition, such as renal disease, obstructive uropathy, human immunodeficiency virus infection, and the effects of medications such as a non-steroidal anti-inflammatory drug, angiotensin-converting enzyme inhibitors, and cyclosporine. Resistance to the action of aldosterone occurs in tubulointerstitial renal disease, pseudohypoaldosteronism, and drugs that close the collecting tubule sodium channel (trimethoprim, pentamidine, amiloride, and spironolactone). Given your patient's history, the most likely culprits include primary aldosterone deficiency, secondary aldosterone deficiency (from an undiagnosed obstructive uropathy), and pseudohypoaldosteronism. Renal US reveals normal kidneys, without signs of obstruction. The definitive diagnostic tests are renin and aldosterone levels and a mineralocorticoid profile, but the results of those tests wouldn't be available for one or two weeks.... The parents are anxious for a diagnosis, and you need a discharge plan that will prevent recurrence of the hyponatremia and vomiting before definitive diagnostic results are available. Wait: There's an indirect way to evaluate aldosterone action, you recall—the transtubular potassium concentration gradient, or TTKG, a calculation that estimates aldosterone activity in the kidney. TTKG is used to evaluate hyperkalemia to determine whether hypoaldosteronism is supported as the cause, and it uses data that are often much more quickly available than measurements of renin and aldosterone. This calculation is generally accurate when urine osmolality is greater than serum osmolality and the urine sodium level is >25 mmol/L (which ensures adequate sodium delivery to the kidney). In a setting of hyperkalemia with an appropriately elevated aldosterone level and renal collecting tubule potassium secretion, TTKG is high when it exceeds 10. A TTKG value of <7 and, especially, <5 strongly supports hypoaldosteronism. You perform the calculation and determine that your patient's TTKG is 4.98—hypoaldosteronism it is. You discharge the boy on sodium chloride supplementation and give his parents a prescription for fludrocortisone, to be filled if follow-up blood chemistry tests show hyponatremia despite sodium chloride supplementation—pending results of the definitive tests, of course. More than a week later, test results are in your hands: Plasma renin activity is elevated at 190,881 ng/dL/h (normal, 235-3,700 ng/dL/h at 1 to 11 months of age) and aldosterone is inappropriately low (in a setting of hyponatremia) at 7 ng/dL (normal, 5-90 ng/dL at 1 to 11 months). A mineralocorticoid profile reveals elevated corticosterone and 18-hydroxycorticosterone levels with a normal deoxycorticosterone (DOC) level. Because of elevated precursors to aldosterone in the setting of inappropriately low-to-normal aldosterone and hyperreninemia, this patient's profile is consistent with an isolated deficiency of the enzyme aldosterone synthase (AS), formally known as P450c11AS. Because of the patient's elevated ratio (>100) of serum 18-hydroxycorticosterone to aldosterone, the profile is consistent with a specific mutation in AS that deletes 18-methyl oxidase activity but preserves 18-hydroxylase activity—a condition known as corticosterone 18-methyl oxidase deficiency type II (CMO type II) Aldosterone synthase is present only the zona glomerulosa of the adrenal gland. Deficiency is a rare autosomal recessive condition most common in Iranian Jews but also documented throughout Europe and North America. Clinical presentation varies by age. Affected infants typically have recurrent dehydration, hyponatremia, hyperkalemia, and mild metabolic acidosis. Hyponatremia manifests as nausea, vomiting, weakness, and, at the extreme, seizures and altered mental status. Salt wasting is less severe than in typical congenital adrenal hyperplasia brought on by 21-hydroxylase deficiency because of the production of DOC, which has a mineralocorticoid effect. Older children with a deficiency of AS may have anorexia, poor growth, and mild dehydration. Symptoms tend to wane with age (as the renin level falls)—sometimes, even without therapy because of the increasing sensitivity of mineralocorticoid action that occurs over time. An abnormal ratio of 18-hydroxycorticosterone to aldosterone may be the sole biochemical abnormality in adults with this disorder. Adults are usually asymptomatic, although they may not be able to tolerate salt loss with illness that is associated with gastrointestinal fluid losses. Hypertension may also be seen (as it is in other hyperreninemic conditions) because of increased production of the vasoconstrictor angiotensin II. Hypertension resolves with correction of hyponatremia and hypovolemia, leading to a lower renin level. Treatment of an infant who has AS deficiency involves oral sodium chloride supplementation (1-2 g/day) and fludrocortisone (0.1-0.3 mg/day). Catch-up growth is usually rapid after hyponatremia and dehydration are corrected. Mineralocorticoid replacement therapy should be maintained throughout childhood until growth is complete. Your patient was started on oral sodium chloride supplementation at 1 mmol/kg of weight three times a day at first, tapered to twice a day, and oral fludrocortisone, 0.2 mg/day. Vomiting ceased upon correction of hyponatremia, after which he tolerated a standard milk-based infant formula. He gained 0.9 kg over the first three weeks , and BP normalized. Lab tests demonstrated normalization of sodium and potassium levels.
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#66
20.04.2006, 16:26
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Ну, в общем, первая мысль была, конечно, про сольтеряющую форму. Пока читала Нельсона (чтобы выглядеть умнее в глазах коллег и своих собственных
 ), ты повесил продолжение.  Очень красиво - и дифдиагноз, и диагноз! Спасибо! Жду еще.
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#67
21.04.2006, 10:30
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Вести из маленького городка:
Ребенок от 4б, 3р, за неделю до родов мать перенесла ОРЗ (лечилась симптоматически). Вес при рождении - 4650, тугое обвитие пуповиной. 7/8 б. С рождения - стридорозное дыхание, инспираторная одышка 70/мин, втяжение, цианоз (пульсоксиметр в роддоме сломан), беспокойство (ДН 2-3). Единственный педиатр в командировке. Ребенком занимаются акушер и реаниматолог. Поставлен диагноз "СТРАНГУЛЯЦИОННАЯ асфиксия", ввели 25мг преднизолона, кислород маской (попыток интубации не было) - ребенок успокоился, порозовел. Через 4 часа - ухудшение состояния. При прямой ларингоскопии: Слизистая полости рта - без изменений. В области надгортанника - округлое, ярко-малиновое образование 1см в диаметре, плотное, закрывающее вход в гортань. Надгортанник не визуализируется. Связки не изменены. Интубация с техническими труднорстями - клинком ларингоскопа образование с усилием смещено в сторону. Интубирован трубкой #3, дыхание восстановилось, свободное, Sa 90 (FiO2 30). ВЕ - 4, Hb 202, RBC 4.3, WBC 25, Ht 58. Ребенок перевезен в ОРИТ Областной детской больницы. ЛОР, челюстно-лицевые хирурги пока не смотрели. Ваше мнение? Что это могло быть? PS Простите за некоторый сумбур - только что вернулся с дежурства.
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#70
21.04.2006, 11:01
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Признаюсь, я ни разу не видел гемангиом на слизистых. На "кожную" - совсем не похоже. Уж больно правильная, гладкая и круглая. И очень плотная.
Похоже на эпиглоттит. Но я ничего не слышал про врожденные эпиглоттиты. Поиск тоже пока ничего не дал. Вот ищу в интернете и жду, пока ребенка осмотрят узкие специалисты...
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#72
21.04.2006, 11:04
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Цитата:
...забыл добавить - на шее ничего необычного не пальпируется.
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#73
21.04.2006, 11:12
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...Таблица 1
Причины нарушений проходимости гортани Причина нарушения проходимости гортани Распределение больных по возрасту 0-3 (в годах) Общее количество больных Рубцовый стеноз гортани 26 Ларингомаляция 23 Парез голосовых складок 8 Врожденный стеноз гортани 4 Ангиома гортани 5 Киста гортани 3 Папилломатоз гортани - Рубцовый стеноз гортани при химических ожогах гортаноглотки 9 Общее количество больных 78 ... Наиболее вероятным диагнозом, с учетом визуальной картины, вероятно можно считать ангиому, однако киста гортани также может быть взята в расчет при установлении диагноза.
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#74
24.04.2006, 10:18
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последние новости - киста. Реаниматологи видели, а вот ЛОРы уже нет - ушла. Ребенок экстубирован.
При беспокойстве - появляется осиплость (?). Завтра дежурю, уточню.
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Линейный вид
