#succimer

[livealthbiopharma]

https://livealthbiopharma.com/products/succimer-capsules-200mg/

[mcatmemoranda]

I had a 2 year old in clinic today whose lead level was elevated. It was 56 after the nurse checked it twice. This is what UpToDate says about management of elevated lead levels: The only effective long-term treatment is ending further lead exposure by eradication of environmental lead contamination. Because of the cognitive and behavioral effects of lead toxicity, primary prevention of lead exposure is the single most important strategy in the management of childhood lead poisoning.

Children at risk because of lead in their environment are often not found until elevated blood lead levels (BLLs) are detected during routine screening. At that point, secondary prevention of further lead exposure becomes the main treatment:

1) Report to appropriate health authorities (eg, city, county, or state health department)

2) Take emergency measures to reduce lead exposure. Relocate the child and family to lead-free housing if necessary.

3) Initiate intensive blood lead screening and/or chelation as determined by the degree of the child's blood lead elevation.

4) Educate the family about sources of lead exposure so that they can be eliminated

5) Follow-up on long-term abatement procedures by a licensed contractor to reduce lead exposure.

Chelation therapy may be necessary depending upon the degree of blood lead elevation (see 'Lead level 45 to 69 mcg/dL' below and 'Symptomatic lead poisoning' below). However, it has limited efficacy. With chronic ingestion or inhalation, lead can be incorporated into the skeletal system, which becomes an endogenous reservoir of lead that is resistant to elimination. While chelating agents can bind to lead in blood, they are ineffective in removing lead from the deep bone stores.

Lead level 45 to 69 mcg/dL — Asymptomatic children with venous BLLs 45 to 69 mcg/dL (2.17 to 3.33 micromol/L) should have a confirmatory venous lead level within 48 hours. These patients should also receive the same general management as for children with lower levels as described above and listed in the table.

We recommend that asymptomatic children with BLL ≥45 mcg/dL (2.17 micromol/L) receive chelation therapy. Treatment should begin as soon as possible after the BLL is confirmed, and only when the child is in a lead-safe environment. We suggest that chelation be performed orally with succimer (table 6) rather than by continuous infusion of calcium disodium edetate (CaNa2EDTA) or oral penicillamine. If succimer is contraindicated, not tolerated, or causes significant adverse reactions, then CaNa2EDTA is suggested [37]. Chelation should be performed in consultation with a toxicologist or clinician who has experience with the chelating agents.

Ongoing care includes:

●BLLs should be measured weekly at the end of oral chelation until the lead level plateaus to ensure no sudden increase from re-exposure. The interval for testing may be increased once the level plateaus and no ongoing exposure occurs.

●Retreatment with chelation therapy should occur if the BLL rebounds to >80 percent of the original lead level and is ≥45 mcg/dL (2.17 micromol/L).

●An acute rise in levels may signify a new exposure to lead, and repeat evaluation, including a plain abdominal radiograph, and renewed surveillance of the child's environment will be necessary. This is especially true if the "rebound" levels rise above pre-chelation levels.

Symptoms attributable to lead poisoning can include intermittent vomiting, anorexia, and abdominal pain (lead colic); intermittent irritability or lethargy; and/or lead encephalopathy (eg, persistent vomiting, persistent lethargy or coma, headache, or afebrile convulsions)

Symptomatic lead intoxication is a medical emergency warranting an emergency repeat blood lead level (BLL) for confirmation, emergency evaluation, hospitalization, and chelation. Children with lead encephalopathy should be admitted to a pediatric intensive care unit.

Performing a lumbar puncture should be avoided in encephalopathic children unless absolutely necessary to rule out meningitis because lead intoxication can cause increased intracranial pressure. Extreme caution should be exercised if lumbar puncture is attempted, and only a small amount of spinal fluid (less than 1 mL) should be removed.

Succimer — Succimer (meso-2,3-dimercaptosuccinic acid) is a water-soluble analog of dimercaprol (British anti-Lewisite, BAL) that can be administered orally [48,49]. Like dimercaprol and CaNa2EDTA, succimer increases the urinary excretion of lead.

Calcium disodium edetate — In 1950, calcium disodium edetate (CaNa2EDTA), was found to be clinically useful in the treatment of lead poisoning. Like dimercaprol, CaNa2EDTA increases the urinary excretion of lead through the formation of a nonionizing, soluble chelate.

Dimercaprol — Dimercaprol (2,3-dimercapto-1-propanol), also known as British Anti-Lewisite or BAL, was developed in 1946 by the British to counteract German arsenical war gases. It was the first chelating agent found to be useful in the treatment of childhood lead poisoning. Dimercaprol increases the fecal and urinary excretion of heavy metals through the formation of stable, nontoxic, soluble chelates. Dimercaprol lacks stability in water and must be dissolved in peanut oil for deep intramuscular injection.

D-penicillamine — D-penicillamine is another oral chelating agent. It was developed originally to reduce serum copper concentration in patients with Wilson disease [67]. American Academy of Pediatrics (AAP) guidelines for the treatment of lead toxicity describe penicillamine as a third-line agent, indicated only when unacceptable reactions have occurred to succimer or CaNa2EDTA, and continued therapy is required. Given the potential for significant adverse events (including leukopenia, thrombocytopenia, hematuria, abnormal liver function, urticaria, angioedema, Stevens-Johnson syndrome, and nephritic syndrome), use of this agent is not generally recommended and consultation with a clinician with expertise in managing pediatric lead poisoning with D-penicillamine chelation is advised before starting this treatment

[iasuhfiu]

쥐띠 - 한발 물러서 상황을 바라보는 마음의 여유가 필요하다. 조급하게 서두르지 않고 신중함을 가진다면 안 될것 또한 없다. 한박짜 쉬어간다고 생각하라. 48년생 : 오늘 해야 할 일을 내일로 미룬다면 내일이 더 고달파질 수 있다는 것을 알아야 한다. 60년생 : 바라던 도움을 받게 된다. 마음을 편하게 해도 될 것이다. 72년생 : 마음과는 다르게 자꾸 상대를 멀리하게 된다. 84년생 : 어느 쪽을 선택하느냐는 바로 자기 자신에게 달려 있다. 96년생 : 아직은 때가 아니다. 때를 기다리면서 더 많은 준비를 해야 할 것이다. DL-Dimercaptosuccinic acid 분자구조 분자의 화학적 구조는 원자의 배열과 각 해당 원자들 간의 화학결합으로 결정된다. 분자는 6 개의 수소 원자, 4 개의 탄소 원자, 4 개의 산소 원자 그리고 2 개의 황 원자로 구성되어 총 16 개의 원자로 형성된다. 분자에는 총 15 개의 화학결합이 있으며, 이는 9 개의 비수소결합, 2 개의 다중결합, 3 개의 단일결합, 2 개의 이중결합, 2 개의 카르복실산(지방족), 2 개의 수산기 그리고 2 개의 티올로 구성되어 있다. 의 구조 이미지는 아래와 같다.DL-Dimercaptosuccinic-acid 2차원 구조DL-Dimercaptosuccinic-acid 3차원 구조 3차원 분자 모형 및 구조 데이터 DL-Dimercaptosuccinic-acid 3차원 분자모형분자 모형을 회전, 확대, 축소 등 다양한 기능을 통해서 보다 상세하게 살펴볼 수 있다. 추가 메뉴를 통해 반 데르 발스 표면 등을 시각화 하고 이미지 파일로 내보내는 등의 옵션을 활용할 수 있다. 반응형 3차원 구조 모형 바로가기 ]분자의 원자, 화학 결합, 연결성 및 좌표에 관한 정보 등이 포함된 구조 데이터 파일을 다운로드 할 수 있다. 대부분의 주요 화학 소프트웨어에서 지원된다. 구조 데이터 파일 다운로드 바로가기 ] 다른 이름(동의어) 또는 등록번호 DL-Dimercaptosuccinic acid DL-Dmsa DL-2,3-Dimercaptosuccinic acid (2R,3R)-2,3-Dimercaptosuccinic acid Succimer더보기Succinic acid, 2,3-dimercapto-, (+-)- 10008-75-0 C4H6O4S2 DMSA CAS-27887-84-9 27887-84-9 2,3-Dimercaptosuccinic acid, (-)- Succinic acid, 2,3-dimercapto-, (2R,3R)-(-)- K853KBN17Q CCG-37981 Succimer, (R*,R*)-(+,-)-Isomer (2R,3R)-2,3-Dimercaptobutanedioic acid

[harmfulcures4autism-blog]

Harmful Treatment #1: Chelation

Chelation is a chemical process in which a substance is used to bind molecules, such as metals or minerals, and hold them tightly. It is originally used to rid the body of excess or toxic metals. It has some uses in conventional medicine, such as treating lead poisoning or iron overload.

During the process of chelation, a synthetic solution-EDTA (ethylenediaminetetraacetic acid) is injected into the bloodstream to remove heavy metals and/or minerals from the body.

This treatment stems from the idea that vaccines cause Autism, which is an untrue claim with no scientific evidence to back it up. 

Chelation Therapy is used as a treatment for acute heavy metal poisoning in removing metals such as arsenic, lead, and mercury from the bloodstream with the administrating of chelating agents. The medication binds to the heavy metals and then would be filtered out through urine. Chelating agents are nondiscriminating and they will bind to any heavy metal it comes to contact in, which can result in vital metals, such as calcium and iron, to be filtered out of the body alongside with the toxins if administrated incorrectly. There are several different types of Chelating drugs that are used depending on the type of poisoning that has occurred. Each one has its own benefits and risks to it.

The different types include:

Succimer (DMSA, 2,3-dimercaptosuccinic acid) is taken by mouth to treat poisoning by lead, mercury, and arsenic. Serious side effects are uncommon.

Dimercaprol (British Anti-Lewisite, BAL) is given by injection to treat severe lead, mercury, and arsenic poisoning. Side effects are usually dose-related but can cause coma and seizures.

Edetate calcium disodium (CaNa2EDTA) is given intravenously to treat severe lead poisoning. This can be toxic to the kidneys.

Deferoxamine is given intravenously to treat iron poisoning. Possible side effects include very low blood pressure, lung injury, and infections

Penicillamine is sometimes used to treat bismuth, copper, lead, mercury, and nickel toxicity. The primary adverse effect is an allergic reaction in people who are also allergic to penicillin.

There have been several unapproved uses for Chelation Therapy as of late for treatment in the autism spectrum, cardiovascular diseases, Parkinson's disease, Alzheimer's disease, and other serious conditions.

The idea of using Chelation for these purposes is that it is believed that the caused for these disorders are caused by damage from heavy metal poising. For autism, it is believed that the cause may be mercury poisoning from the thimerosal in vaccines.

[mcatmemoranda]

From First Aid for USMLE Step 2 CK

Dimercaprol is a chelating agent (binds to heavy metals).

In a fire, burning textiles generate cyanide. You also are exposed to carbon monoxide in a fire. So for anyone who was in a fire in an enclosed space, check for carbon monoxide and cyanide poisoning.

If someone has cyanide poisoning due to the anti-hypertensive drug nitroprusside, you can treat it with amyl nitrite. But amyl nitrite should not be used to treat cyanide poisoning due to smoke inhalation because amyl nitrite-> methemoglobin, which worsens the carboxyhemoglobinemia that occurs with carbon monoxide poisoning. So if the pt has cyanide poisoning due to smoke inhalation, treat it with thiosulfate.

[azveille]

Prescrire réserve son jugement sur Spinraza* et Bavencio*

La revue Prescrire, dans son numéro d'août, a refusé de se prononcer sur le bénéfice du traitement de l'amyotrophie spinale Spinraza* (nusinersen, Biogen) et de l'anti-PD-L1 Bavencio* (avélumab, Merck KGaA/Pfizer).

L'oligonucléotide antisens Spinraza* est le premier médicament à avoir décroché une autorisation de mise sur le marché (AMM) européenne dans le traitement de l’amyotrophie spinale 5q, en mai 2017, rappelle-t-on. 

Si "la rédaction ne peut se prononcer", c'est que les inconnues concernant les effets indésirables sont "encore nombreuses", malgré une réduction de la mortalité à court terme sans effet important sur le handicap. Prescrire considère qu'il est préférable de réserver Spinraza* à la recherche clinique.   

"Autoriser ce médicament sur la base d'une telle évaluation place les parents et les soignants à la hauteur des incertitudes, car à partir des données disponibles, on ne peut pas déduire ce que vont avoir à vivre les nourrissons traités", souligne Prescrire.  

La revue consacre par ailleurs son éditorial au "prix exorbitant" de Spinraza*, dont le coût de traitement atteint 500.000 euros la première année et 250.000 les suivantes. "Partout dans le monde, le prix monstrueux de certains nouveaux médicaments épuise leur valeur pratique", souligne cet éditorial.

Bavencio* a été homologué en septembre 2017 dans le traitement en monothérapie du carcinome métastatique à cellules de Merkel chez l'adulte. A ce jour, la balance bénéfices/risques est "incertaine", juge Prescrire.

L'essai clinique ne démontre pas que Bavencio* apporte un "avantage clinique concret" par rapport à des soins symptomatiques. Les données ne sont pas comparatives pour attester l'effet antitumoral du produit et le recul est à ce jour insuffisant pour savoir si cela modifie le pronostic ou la qualité de vie des patients, alors que les effets indésirables sont nombreux et parfois graves.

Prescrire juge aussi que l'anticancéreux Tecentriq* (atézolizumab, Roche) "n'apporte rien de nouveau" dans une des deux indications de son AMM initiale concernant le carcinome urothélial localement avancé ou métastatique, chez les patients déjà traités avec une chimiothérapie à base de sels de platine ou considérés comme inéligibles au cisplatine, peu importe le statut de PD-L1. L'autre indication concerne le cancer du poumon non à petites cellules (NAPC), rappelle-t-on.

Dans l'essai clinique, Tecentriq* "n'a pas été plus efficace" sur la mortalité que des taxanes ou la vinflunine (Javlor*, Pierre Fabre), mais il présente toutefois un profil d'effets indésirables potentiellement plus faibles.

Prescrire juge que Stelara* (ustékinumab, Janssen, groupe Johnson & Johnson) n'apporte rien dans le traitement de la maladie de Crohn active modérée à sévère chez les patients adultes présentant une réponse insuffisante, une perte de réponse ou une intolérance à un traitement conventionnel ou par anti-TNF alpha ou qui présentent une contre-indication médicale à ces traitements.

Stelara* n'a pas été comparé à un anti-TNF alpha et, en cas d'échec avec un produit de ce type, il entraîne une rémission clinique seulement chez une minorité de patients sans prouver un maintien de cet effet à long terme. Les effets indésirables sont nombreux et parfois graves.

Améliorations dans la "vraie vie"

L'insuline aspart à action ultra-rapide Fiasp* (Novo Nordisk) n'apporte rien de nouveau car le délai d'action est réduit de cinq minutes par rapport à NovoRapid*, sans preuve que cette différence apporte un progrès en cas d'injection après un repas.

Prescrire a évalué deux fois Trolovol* (D-pénicillamine, Erempharma) dans son numéro d'août:

il est "éventuellement utile" dans le traitement de la cystinurie (extension d'AMM obtenue fin 2016) car il constitue une alternative à Acadione* (tiopronine, Sanofi) qui a cessé d'être commercialisé, malgré une évaluation jugée pas assez rigoureuse

mais la revue n'est "pas d'accord" pour son extension d'AMM de 2016 dans le traitement de l’intoxication au plomb car son efficacité semble inférieure à Succicaptal* (succimer, SERB) et son profil d'effets indésirables est "plus préoccupant", sans qu'une formulation soit adaptée aux enfants.

Les antihypertenseurs à base d'olmésartan Alteis* et Olmetec* (Daiichi Sankyo) ont écopé de la mention "pas d'accord" dans leur indication pédiatrique car la balance bénéfices/risques est négative et les effets indésirables nombreux.

La nouvelle formulation buvable de l'enzyme de conversion captopril Noyada* (Martindale Pharma) apporte quelque chose car elle permet une "adaptation précise" des doses et facilite l'administration.

La chronique "Le mot de Gaspard" est consacrée à cette nouvelle présentation: si les autorités sanitaires ne voient pas toujours les améliorations qui rendent plus pratiques dans la "vraie vie" certains médicaments, cela n'en constitue pas moins un progrès.

La nouvelle présentation du traitement de la fibrose pulmonaire idiopathique Esbriet* (pirfénidone, Roche) en comprimés à 267 mg et 801 mg n'apporte rien de nouveau car ils sont équivalents aux gélules, soit gros à avaler et avec une balance bénéfices/risques de la pirfénidone incertaine.

Prescrire a aussi considéré que le premier traitement à base de plantes avec le statut de médicament indiqué dans les troubles du climatère liés à la périménopause Fémélis* (Sérélys Pharma) n'apporte rien de nouveau "faute de données cliniques spécifiques" empêchant de savoir si les femmes sont soulagées d'une gêne liée à la ménopause ou d'un syndrome prémenstruel. Des réactions allergiques peuvent survenir.

Le numéro d'août de Prescrire consacre par ailleurs des articles ou dossiers aux lithiases vésiculaires d'origine médicamenteuse, à la désensibilisation de la rhinite allergique saisonnière, aux morsures de chien ou de chat, aux critères combinés dans les essais cliniques, à l'évaluation des technologies de santé et aux IVG médicamenteuses.  

[khamgiodau]

NGỘ ĐỘC CHÌ Ở TRẺ EM

PHÁC ĐỒ ĐIỀU TRỊ NGỘ ĐỘC CHÌ Ở TRẺ EM

I. CHẨN ĐOÁN

1. Trẻ có tiếp xúc với chì

• Gia đình làm bình ăc quy, nấu chì.

• Sơn có chì, ngâm đồ chơi có sơn chì.

• Thuốc nam, thuốc cam.

2. Lâm sàng

• Ngộ độc mạn: đau bụng, kém ăn suy dinh dưỡng, viền răng đen (đường viền Burton), thiếu máu, cao huyết áp, viêm thận mô kẽ.

• Bệnh lý não cấp: rối loạn tri giác, co giật, hôn mê, tăng áp lực nội sọ.

3. Cận lâm sàng

• Phết máu: thiếu máu nhược săc, basophic stippling trên hồng cầu, tăng hồng cầu lư���i.

• X-quang đầu xương dài: đường viền chì ở đầu xương dài, vùng sụn tăng trưởng.

• Nồng độ chì trong máu tĩnh mạch: > 10 μg/dL.

• ALA/nước tiểu > 13 mg/L.

• Dịch não tủy:

- Do nguy cơ tụt não nên chỉ chọc dịch não tủy trong các ca bệnh não cấp không có phù gai thị cần chẩn đoán phân biệt viêm màng não.

- Dịch não tủy: áp lực ↑, Protein ↑, tế bào bình thường hoặc tăng nhẹ <100/mm3.

• Chức năng thận trước khi dùng EDTA (Calcitetracemate disodique), EDTA chống chỉ định khi có suy thận).

II. PHÂN ĐỘ NGỘ ĐỘC CHÌ

• Ngộ độc chì nặng:

- Lâm sàng: bệnh lý não cấp, hôn mê co giật,tăng áp lực nội sọ, phù não,

- Xét nghiệm: nồng độ chì máu > 70 μg/dL.

• Ngộ độc chì trung bình:

- Lâm sàng: tăng kích thích, quấy khóc, lừ đừ.

Nôn ói, đau bụng, chán ăn.

Thiếu máu.

- Xét nghiệm: nồng độ chì máu 45 - 70 μg/dL.

• Ngộ độc chì nhẹ:

- Lâm sàng: không triệu chứng lâm sàng.

- Xét nghiệm: nồng độ chì máu 10 - < 45 μg/dl.

III. CHẨN ĐOÁN XÁC ĐỊNH

Có tiếp xúc với nguồn chì hoặc có triệu chứng gợi ý. Nồng độ chì trong máu tĩnh mạch: > 10 μg/dL.

IV. ĐIỀU TRỊ

Nguyên tắc điều trị:

• Cách ly bệnh nhi ra khỏi môi trường tiếp xúc với chì.

• Thuốc tăng thải chì.

• Điều trị biến chứng.

Điều trị:

• Cách ly bệnh nhi ra khỏi môi trường tiếp xúc với chì.

• Thuốc tăng thải chì.

• Cách dùng thuốc thải chì:

- Mục tiêu: chì máu < 20 μg/dL và ổn định (hai lần xét nghiệm cuối cùng cách nhau 3 tháng).

- Cách dùng:

+ Dùng theo đợt:

❖ BAL, EDTA: 3 - 5 ngày/đợt.

❖ Succimer: 19 ngày/đợt.

❖ D-penicillamin: 7 - 30 ngày/đợt, theo dõi nếu không có tác dụng phụ thì dùng tối đa 30 ngày/đợt, tạm ngừng hoặc giảm liều ngay khi có tác dụng phụ.

+ Khoảng thời gian nghỉ:

❖ Dùng BAL, EDTA: sau đợt 1 nghỉ 2 ngày, sau đợt 2 nghỉ 5 - 7 ngày, các đợt sau có thể dài hơn tùy theo nồng độ chì máu.

❖ Succimer: thường nghỉ ít nhất 2 tuần trước khi dùng thuốc đợt tiếp theo.

❖ D-penicillamin: bệnh nhân có triệu chứng nhẹ, nghỉ 10 - 14 ngày trước khi băt đầu đợt tiếp theo, các đợt nghỉ 14 ngày.

- Không sử dụng thuốc thải chì nếu nồng độ chì < 20 μg/dL. Riêng đối với trẻ > 2 tuổi, không sử dụng thuốc thải chì nếu nồng độ chì < 45 μg/dL.

- Nồng độ chì từ 10 - 20 μg/dL (trẻ < 2 tuổi) hoặc từ 10 - 44 μg/dL (trẻ > 2 tuổi): theo dõi, tái khám xét nghiệm nồng độ chì trong máu mỗi tháng đến khi nồng độ chì <10 μg/dL.

Mức độ ngộ độc chì

Thuốc

Liều lượng

Ngộ độc chì nặng (nồng độ chì máu > 70 μg/dl)

BAL kết hợp EDTA (sau BAL 4 giờ) trong 5 ngày mỗi đợt.

BAL: Tiêm bắp

- Ngày thứ 1 và 2: 2,5 - 3 mg/kg/lần mỗi 4 giờ

- Ngày thứ 3: 2,5 - 3 mg/kg/lần mỗi 6 giờ

- Ngày thứ 4 và 5: 2,5 - 3 mg/kg/lần mỗi 12 giờ.

EDTA: 1500 mg/m2 da/ngày, hoặc 50-75 mg/kg/24 giờ chia làm 4 lần, pha với Normal saline truyền TM trong 1 giờ

Ngộ độc chì trung bình (nồng độ chì máu 45 -70 μg/dL)

EDTA trong 5 ngày mỗi đợt.

Hoặc DMSA trong 19 ngày mỗi đợt

EDTA truyền TM như ngộ độc nặng DMSA uống

- Từ ngày thứ nhất đến ngày thứ 5: 10 mg/kg mỗi 8 giờ

- Sau đó từ ngày 6 đến ngày 14: 10 mg/kg mỗi 12 giờ

Ngộ độc chì nhẹ (nồng độ chì máu 10 -< 45 μg/dl)

D - penicilamin trong

1 tháng.

Hoặc DMSA trong 19 ngày mỗi đợt

D - penicilamin

- Băt đầu 10 mg/kg/ngày mỗi 8 giờ trong 2 tuần

- Sau đó 25 - 30 mg/kg/ngày trong 2 tuần

- Uống trước bữa ăn

DMSA uống như ngộ độc trung bình

• Hai tuần sau đợt điều trị: xét nghiệm lại nồng độ chì trong máu nếu còn ngộ độc có thể lặp lại đợt điều trị thứ hai.

• Điều trị biến chứng:

- Hỗ trợ hô hấp

- Chống phù não:

+ Tăng thông khí nhằm giữ PaCO2 25 - 30 mmHg.

+ Mannitol.

+ Furosemid, Dexamethason.

- Chống co giật: Diazepam tiêm tĩnh mạch.

- Hạn chế dịch, điều chỉnh rối loạn điện giải.

.Bài viếtNGỘ ĐỘC CHÌ Ở TRẺ EM xuất hiện lần đầu tại website http://khamgiodau.com

[vetschoolhaiku]

A haiku on lead poisoning

Red cells get stippled Chelate lead with succimer Consider the source

[mcatmemoranda]

Lead interferes with numerous bodily processes and affects various organ systems including cardiovascular, nervous, hematopoietic and renal systems. Young children are most commonly exposed to lead through lead based wall paint in their homes, while adults are most commonly exposed due to occupational exposures. Manifestations of acute poisoning can vary and either be asymptomatic or can include symptoms such as altered mental status, seizures, motor weakness, abdominal pain, vomiting, constipation, headaches, ataxia, somnolence and weakness secondary to hemolytic anemia. History of exposure whether environmental or occupational is vital to making the diagnosis. The combination of any neurological abnormalities, abdominal pain and hemolytic anemia should increase the suspicion for this diagnosis. The definitive diagnosis is made with a serum blood lead level. Levels that are greater than 10 µg/dL is considered elevated. The three therapies available for the treatment of lead toxicity include chelation therapy with dimercaprol, edetate calcium disodium, or succimer. The choice of chelation therapy is based on the patient's age, serum lead levels, and symptom manifestation.

Bottom Line: When suspecting the diagnosis of lead poisoning, the serum lead level is the most important diagnostic modality.

[mcatmemoranda]

This is one of the handouts parents get if their kids have high lead levels. It's called "Lead and Nutrition."

In NH, children are screened for lead poisoning at ages 1 and 2 with the finger prick test. If the level is high, they need a blood draw to confirm the lead level (venous blood draw).

Parents should wet mop floors and windowsills, clean children's pacifiers and toys, wash kids's hands often.

Ask parents about behavioral problems, developmental delays/disabilities, excessive mouthing (putting keychains in mouth; items like that could have lead in them)/pica (eating non-nutritional items), whether housing was built prior to 1978, whether their child-care facility was built before 1978, whether their housing has renovations, whether the child is a recent refugee/immigration/international adoption, whether parents' job could expose them to lead (welding, renovating, painting, fishing, stain glass, target shooting, jewelry making), whether they imported any spices that could contain lead (turmeric, sindoor, surma, orange shringar, asafetida).

You need to do annual developmental surveillance and may refer for early childhood education/stimulation programs.

When you screen for lead in office with the finger prick, you have to wash the child's hands with soap and water first.

Symptoms of lead poisoning include stomach aches, headaches, trouble paying attention, developmental delays, behavior issues, problems eating and sleeping, speech/language delays.

Long term effects: slowed growth, poor school performance, hyperactivity, aggression, brain/kidney/nerve damage.

Home, water, and soil should be tested for lead.

Parents should feed children foods high in calcium, iron, and vitamin C.

Tx of high enough BLL: chelation with succimer of calcium disodium edetate. Succimer — Succimer (meso-2,3-dimercaptosuccinic acid) is a water-soluble analog of dimercaprol (British anti-Lewisite, BAL) that can be administered orally [48,49]. Like dimercaprol and CaNa2EDTA, succimer increases the urinary excretion of lead. Like dimercaprol, CaNa2EDTA increases the urinary excretion of lead through the formation of a nonionizing, soluble chelate.

Symptoms attributable to lead poisoning can include intermittent vomiting, anorexia, and abdominal pain (lead colic); intermittent irritability or lethargy; and/or lead encephalopathy (eg, persistent vomiting, persistent lethargy or coma, headache, or afebrile convulsions)

From UpToDate:

EMERGENCY MEDICINE (ADULT AND PEDIATRIC) (November 2021)

New threshold for elevated blood lead in United States children

●For children younger than six years of age in the United States, the reference value for an elevated blood level is 3.5 mcg/L (0.17 micromol/L).

Detectable blood lead levels (BLLs) are associated with neurocognitive deficits in infants and children less than 6 years old, and targeted screening of at-risk children is recommended. The Centers for Disease Control and Prevention has lowered the blood lead level (BLL) threshold for action to 3.5 mcg/dL (0.17 micromol/L) from the previous level of 5.0 mcg/dL (0.24 micromol/L) [1,2]. At or above this threshold, specific interventions should be taken based upon the degree of BLL elevation. For children with BLLs below 3.5 mcg/dL, the limit of detection for lead varies by laboratory, and the actual blood lead value may be close to or above the threshold. Thus, some children may need to be retested depending upon age or other risk factors.

With chronic ingestion or inhalation, lead can be incorporated into the skeletal system, which becomes an endogenous reservoir of lead that is resistant to elimination. While chelating agents can bind to lead in blood, they are ineffective in removing lead from the deep bone stores.

I had twin pts who both had EBLL of 5 mcg/dL in August and level of 4 mcg/dL today. One of them hadn't grown as much as her twin, so there was concern that the EBLL might be affecting her growth. Scheduled both pts for f/u with repeat venous BLL, CMP, iron level, CBC in 3 months.

Tx: BLL less than 45 mcg/dL = no need for chelation; get abdominal X-ray if pt has signs of excessive mouthing (puts everythin in their mouth) or pica (eats non-food items). If you see lead chips, can do whole bowel irrigation. Clean the home and toys. Make sure kids get 5 servings veggies and fruits a day with vitamins including iron. Wash their hands. If BLL is greater than 45 mcg/dL, chelation is necessary.

[mcatmemoranda]

Lead poisoning can be caused by the ingestion of paint chips, consumption of moonshine made in lead-lined radiators, and working in factories that use lead-containing casting materials such as battery or ammunition factories. Many toxic substances can have similar symptoms such as abdominal pain, nausea, vomiting, and diarrhea. Common long-term exposure symptoms including chronic abdominal pain, distal sensorimotor neuropathy, and microcytic anemia.

Lead denatures enzymes involved in hemoglobin synthesis such as ferrochelatase, ALA dehydrase, and ribonuclease, which can lead to laboratory abnormalities including hypochromic, microcytic anemia with basophilic stippling of red blood cells. Lead poisoning leads to acute and chronic symptoms depending on the time and amount of exposure but is commonly associated with abdominal pain, diarrhea, encephalopathy, peripheral neuropathy (more commonly motor, but can be sensory as well), and renal failure. Lead poisoning is best treated with chelating agents such as succimer or dimercaprol, but the definitive treatment involves removing the source of exposure.

Arsenic poisoning causes nausea, vomiting, diarrhea, abdominal pain, garlic odor of breath and stool, QTc prolongation, shock, ARDS; chronic arsenic poisoning causes hyperpigmented and hypopigmented skin lesions, hyperkeratosis of skin, Mee's or Beau's lines (on nails), symmetrical sensorimotor polyneuropathy. Exposures include: contaminated drinking water via pesticides, pressure-treated wood, semiconductors, fuel combustion, metallurgy, smelting.

Mercuty poisoning causes stomatitis, inflammation of the gums, nausea, vomiting, diarrhea, conjunctivitis, dermatitis. Chronic symptoms incude: neuropsychiatric features including anxiety, irritability, insomnia, depression, tremor, pathologic shyness, memory loss. Exposure to organic mercury: swordfish, shark, mackerel, tuna. Exposure to elemental mercury: smelting operations, electroplating operations, tooth fillings in dental offices.

The antidote to all of these is chelating agents: succimer, dimercaprol

The 2 tests for latent TB are the tuberculin skin test using purified protein derivative (PPD) and the interferon-gamma release assay. Both tests look for an immune reaction to mycobacterial antigens, which requires prior or ongoing infection. Both tests will be positive with either active or latent TB, and neither test can tell the difference between them. The first step after a positive PPD test or interferon-gamma release assay is to determine if there is ongoing active TB. This step is usually done through history and examination and with limited imaging, such as a chest x-ray. If active TB is ruled out, treatment for latent TB is recommended if the risks of treatment are outweighed by the risks of reactivation. In all cases, these risks and benefits of treatment should be discussed with the patient. In general, treatment does not cure latent TB, but it significantly decreases the risk of eventual reactivation.

The more immunosuppressed a person is, the smaller the area of induration needed for a positive test. This approach is based on the idea that with escalating immunosuppression, the reaction to the antigen will be less, leading to a smaller reaction.

[mcatmemoranda]

Lead poisoning is the most common environmental illness in children in the United States. Most exposure in children is due to lead-contaminated household dust from leaded paints. Most adult cases of lead poisoning are due to occupational exposure (employees in storage battery manufacturing and lead and zinc ore mining industries). Symptoms are usually subtle and may include increased irritability, headaches, hyperactivity or lethargy, intermittent abdominal pain, vomiting, and/or peripheral neuropathy. Physical examination may show signs of iron deficiency anemia (common in children with lead poisoning), and neurological deficits (diminished deep tendon reflexes, weak extensor muscles). Whole blood lead levels (BLL) should be obtained in all patients with suspected lead poisoning. Then, a plain x-ray of the abdomen should be performed in all children to detect lead-containing objects. Retained lead objects in the GI tract are considered a medical emergency and require referral for possible removal. Further management depends on the patient’s BLL level. Environmental investigation and follow-up testing is required for children with BLLs of 10 µg/dL or higher. Chelation therapy with either oral succimer (DMSA) or IV ethylenediaminetetraacetic acid (EDTA) is warranted in patients with BLLs greater than 45 µg/dL.

Bottom Line: The initial step in the work-up of suspected lead poisoning is to obtain a whole blood lead level (BLL). A plain film radiograph of the abdomen is recommended in children to detect retained lead objects that may require surgical intervention for removal.

[mcatmemoranda]

The three therapies available for the treatment of lead toxicity include chelation therapy with dimercaprol, edetate calcium disodium, or succimer. The choice of chelation therapy is based on the patient’s age, serum lead levels and symptom manifestation.