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15 y/o boy has dysphagia for 2 days

15 y/o boy has dysphagia for 2 days. 臺大醫院 小兒科 張鑾英醫師. Patient data. Name: 吳 Xx Age: 15 y/o Patient No.: 5572797 Birthday: 1994/07/04 Residence : 桃園縣桃園市 Occupation :student Admission date: 2010/05/12 Chief complain :Progressive dysphagia for 2 days. Past History.

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15 y/o boy has dysphagia for 2 days

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  1. 15 y/o boy has dysphagia for 2 days 臺大醫院 小兒科 張鑾英醫師

  2. Patient data • Name: 吳Xx • Age: 15 y/o • Patient No.: 5572797 • Birthday: 1994/07/04 • Residence :桃園縣桃園市 • Occupation :student • Admission date: 2010/05/12 • Chief complain :Progressive dysphagia for 2 days

  3. Past History 1. Birth history:: G3P3, NSD, GA 39 wk, Birth BW 3100gm, perinatal asphyxia (-). Perinatal insult(-) 2. Admission history: admitted once in 2+y/o due to fever 3. Surgical history: Nil 4. Vaccination: H1N1(1) last year 5. Allergies: Denied drug and food allergy 6. Current medication: nil 7. TOCC: T: travel history: denied O:occupation : high school student C:contact : nil, he had a pet dog at home C:cluster : nil

  4. Present Illness Dry cough, sore throat 0507

  5. Present Illness To one 新店H visit his grandmother 0507 0509

  6. Present Illness Fever, dysphagia, ptosis , facial palsy 0507 0509 0510

  7. Present Illness ENT OPD, arrange admission , Oxygen demand, due to downhill situation, Transfer suggested 0507 0509 0510 0511

  8. Transfer to our hospital • 2010/05/11 23:00 NTUH ER T/P/R:37/80/18, SPO2:96%,BP:125/72 Consciousness: clear ,oriented drooping eyelids (+),double vision(-), dysphonia (+), dyspagia (+) no weakness of limbs after muscle use no unusual food exposure history • Transfer to PICU

  9. Physical Examination BH:170 cm BW:50 kg vital signs : T:37.1 P:95 R:18 BP:124/60 mmHg Pain:0 1.General appearance: ill-looking 2.Consciousness: clear, Activity: poor, Appetite: poor, due to dysphagia 3.HEENT: gross anomaly(-); Conjunctiva: not pale; Sclera: anicteric; Pupils: isocoric, Light reflex: +/+, prompt; Throat: sluggish pharyngeal arch elevation, injected(-); ulcer(-); ED: bilateral intact, Neck: supple, LAP(-)

  10. Physical Examination 4.Chest: symmetric expansion, no retraction; BS: coarse, diffuse rhonchi(+), rales(-) 5.Heart: RHB, no murmur 6.Abdomen: soft and flat, normoactive bowel sound, tenderness(-), rebound pain(-) L/S: impalpable 7.Extremity: freely movable, cyanosis(-), pitting edema(-) 8.Skin: rash(-), petechiae(-), ecchymosis(-) wound(-)

  11. NE at ED Cranial nerve: • II : light reflex (+/+), pupil size:3.5 mm/3.5mm • III ,IV, VI : ptosis, fair Extraocular Motility—EOM limitation later • V :no facial numbness, • VII: bilateral facial palsy, no facial expression • VIII: normal • IX ,X :no uvula deviation, gag reflex(+) sluggish pharyngeal arch elevation • XI : weak left trapezius muscle • XII :Protrude tongue : fail • Muscle tone DTR + 5 5 + 5 5 5 + 5 + 5 5

  12. Initial assessment • Septic workup and lumbar puncture • Intubation for airway function security

  13. Lab data

  14. Lumbar puncture

  15. Initial impression • Suspect brain stem encephalitis- less likely Guillain-Barre or Miller-Fisher syndrome- Less likely Neuromuscualr junction dysfunction • suspected myasthenia gravis generalized form- less likely • suspected Botulism • Aspiration pneumonia

  16. 0512 0512 ETT CXR

  17. Brain MRI 5/12: • no definite structural anomalies, no focal signal changes ,no evident abnormal mass effects on the brain parenchyma • Bilateral sinusitis

  18. Clinical course-1 • 5/12 inform CDC for possible botulism poisoning Send patient serum to CDC before Antitoxin injection Gave Botulism Antitoxin (Equine) Types A,B,E No serum sickness during the injection • 5/13 DC sedation Neostigmine test (-) - - 4 3 - - - - 5 5

  19. Clinical course-2 • 5/14 Mouse bioassay Botulism, type A confirmed • history • clinical exam • Demonstrating the presence of toxin in serum ? Culturing C. botulinum from stool, wound or food • Signs of botulism in mice begin with ruffling of the fur followed in sequence by labored abdominal breathing, weakness of the limbs, and total paralysis. Death is caused by respiratory failure

  20. Clinical course-3 1-2 1-2 • 5/15-17 muscle power: limb weakness aggravated EOM: still abducens palsy constipation persisted keep observation &recheck Botulism toxin (antitoxin half-life : 5 to 8 days) 3-4 3-4 4 4

  21. Clinical course-3 • 5/19 CDC: still serum toxin existed give third dose of antitoxin • 5/20:ptosis improved, add Mestinon • 5/22:able to play video • 5/28: (D16) 5 5 4 4 4 4 5 5 5 5

  22. Brief history summary • Acute onset of descending flaccid paralysis in a proximal to distal pattern • Botulism, type A, poisoned food source unknown • Third dose of antitoxin • Respiratory effort improve gradually Muscle power recovering Extubation? antitoxin antitoxin 5/12 5/19 5/24 06? admission

  23. Current problems • Dysphagia , poor cough effort ,high risk of aspiration • Ptosis, abducens palsy • Limb weakness

  24. Lessons from this case • No cluster • Third dose is needed if symptoms progress

  25. Botulism in Taiwan ~Internaional J of Hygiene and environmental health, 2009 82-86, China medical university of hospital, Taichung veterans general hospital

  26. Botulism in Taiwan • Botulism cases in 2007、2008、2009 was 8,11,1 • In 2010, 6 cases, 5/6 confirmed, 1/6 highly suspect • Food-borne 4/6 • Unknown source 2/5 • 52 cases in 25 years(1986-2010) • Less than 10 cases/annually

  27. Pathogenesis Botulism toxin Absorbed form mucosa (gut or lung) or wound Blood Peripheral cholinergic synapses, mainly NMJ Bind irreversibly!! The toxin was internalized and enzymatically blocks Ach release! Weeks to months New motor axon twigs that sprout to re-innervate paralyzed muscle fibers Recovery

  28. Mechanism of botulinum toxin JAMA 2001 Feb 28 vol 285,No.8 1058-2081

  29. Typical presentation Difficulty seeing, speaking, swallowing Typical N.E findings ptosis,diplopia, blurred vision, enlarged or sluggish reactive pupils, dysarthria, dysphagia, dysphonia Sensory sparing! Circumoral or peripheal paresthesia may related to hyperventilation syndrome(firghtened) ~JAMA 2001 Feb 28 vol 285,No.8 1058-2081

  30. Diagnosis of botulism • Stool and food culture • Serous toxin type identification by the mouse inoculation test (mouse bioassay)

  31. Treatment of botulism • Detoxincation • Activated charcoal, enema • Antitoxin • Supportive care and prevention of complication • Fluid and nutrition support • Assisted ventilation • Treatment of secondary infection • Avoid agents that compromise NMJ function • Antibiotics as: aminoglicosides, clindamycin

  32. Botulinum antitoxin • Should be given as soon as possible once clinical suspected • P’t who did not receive antitoxin within 12hrs 3x more likely to develop respiratory failure in one report • There are 2 botulism antitoxin • Trivalent (antineurotoxin-A,B,E) • Equine product (horse-derived antitoxin) ,usually used currently • Heptavalent (antineurotoxin-ABCDEFG): available in US army only • Less immunogenic • Antitoxin binds only to free circulatory toxin • prevent symptoms progression • cannot reverse symptoms • Side effects • Anaphylaxis • Serum sickness ~2001,Chest 120, 562–566.

  33. Trivalent antitoxin (equine antitoxin) • Type A (750IU/ml), TypeB(500IU/ml), TypeE(50IU/ml),250ml/btl • Half life: 5-8 days • Administration • 250ml IVD • 20ml IT (replace 20ml CSF by antitoxin): in patients with no response to IVD antitoxin

  34. Special consideration of botulism • In wound botulism • Antitoxin • Wound I&D with antibiotics (penicillin G) treatment • In infantile botulism • Avoid antitoxin!! • due to risk of anaphylaxis • Give Human botulism immunoglobulin • Antibiotic • did not improve the baby faster, only need if secondary bacterial infection is suspected

  35. Prevention of botulism • Destroy spore • Virtually impossible • Preventing spore fermination • Maintain food in low acid (PH<4.5) • Or storage at 4℃ or colder • Destroy the preformed toxin • Heating the food at 80 ℃ for 20mins • Prevent infant botulism • Avoid honey in children <1y/o

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