Anticoagulant Poisoning Case 3

Clinical Toxicology Laboratory

Group 2 Arcilla, Cheyenne Flores, Mariel Madlambayan, Marianne Janelle Paras, Roxanne

Submitted to: Ms. Marian Elevera, RPh Ms. Reeva Ann Sumulong, RPh

January 24, 2012

Assessment of the Case Age: 30 years old Gender: Male History and presenting complaints He was complaining of diffuse bruises on his skin and blood in the urine. Although the patient had no significant past medical history and on no medications, he reported being depressed and having ingested four packets of rodenticides 8 days prior to presentation. He was well 4 days after the ingestion when symptoms begin to appear. Signs and Symptoms observed Fatigue Weakness Blood in the urine

Laboratory tests with Interpretations Based on the Case Vital sign Temperature Blood Pressure Heart rate Respiratory rate Obtained Value 36.9C 98/50 mmHg 86bpm 14bpm Normal Value 98.6F or 37C 120/80mmHg 60 to 100 bpm 1220bpm Interpretation Normal Hypotension Normal

No orthostatic changes in vital signs. Skin many ecchymoses of slightly different ages, no petechiae Head, Ears, Nose, Eyes and Throat Unremarkable Pallor of the conjunctivae Neck Suppleand without Adenopathy or Thyromegaly Back non-tender Chest clear to auscultation and percussion Heart and Abdomen Unremarkable Neurological Evaluation Within Normal limits Rectal Examination Stool was brown, (+) Occult Blood

Complete Blood Count Obtained Value 9.8 g/dL Normal Value Interpretation Normal

Hemoglobin Prothrombin Time Partial Prothrombin Time Platelets

420,000 platelets/mm3

Normal

Name of poison

Sources

Pharmacology and Metabolism

MOTA

Clinical effects S/Sx

Anticoagulant Rodenticide

The ideal anticoagulant drug would prevent pathologic thrombosis and limit reperfusion injury, yet allow a normal response to vascular injury and limit bleeding. Theoretically this could be accomplished by preservation of the TF-VIIa initiation phase of the clotting mechanism with attenuation of the secondary intrinsic pathway propagation phase of clot development.

Regardless of their classification, all anticoagulants work by inhibiting the generation of an active form of vitamin K1 via inhibition of vitamin K1 reductases. Activation of clotting factors II, VII, IX, and X require the presence of vitamin K as a cofactor. When vitamin K cannot be regenerated, clotting factors cannot be activated and a coagulopathy results involving both the extrinsic and intrinsic pathways (3). The ratio of vitamin K1 2,3-epoxide to vitamin K1 is increased because the inactive compound cannot be reduced back to the active parent form. This ratio has also been documented to be increased in human overdoses (5,6).

Diagnostic test to be monitored in case of poisoning Complete Blood Count Electrolytes ECG Glucose Chest Radiograph

Specific Patient Need Reduction of the Anticoagulant Poison Cure depression of the Patient

End goal

Recommendation

REFERENCE: http://www.medterms.com/script/main/art.asp?articlekey=15737 http://www.iowapoison.com/index.asp?pageID=150 Basic and Clinical Pharmacology 10th edition by Bertram G. Katzung