The male patient, 58 years old, had a nosebleed on the right side before January 28, 22 without obvious precipitating causes, and could not stop himself, so he went to the emergency department of our hospital on the 29th. Emergency department electrocoagulation to stop bleeding and anterior nostril tamponade can not stop bleeding, emergency department is intended to "nosebleed" to receive OTOL.
One
Case after
The attending physician's rounds showed that the patient's hands were broken and bleeding in multiple places.
Emergency blood clots suggest:
PT 158.6s、APTT 110.8s、INR 14.53、WBC 12.7×1012/L、HGB 115g/L、TP 56g/L、Alb 34.2g/L、Urea 19mmol/L，余均正常。
Hematology Society:
Monitoring coagulation elephant q4h, it is recommended to give vitamin K130mg plus 100ml intravenous drip, check ENA + ANA, thyroid function, check for drug factors and toxic factors may be possible, and currently consider acquired coagulation dysfunction.
Past History:
In April 2021, due to "dizziness and gibberish for 4 days", he was hospitalized in the Neurology Department of our hospital for diagnosis and treatment, and the discharge diagnosis was: 1. metabolic encephalopathy, 2. multiple luminal infarction, 3, hypertension grade 1 (extremely high risk). Plain alcoholism, average 7 pairs per day. In September 2021, he was treated with alcohol poisoning in our hospital. History of surgical trauma: History of nasal surgery more than 30 years ago (details unknown).
The main results of each coagulation test are shown in the table below
Inspection Department Treatment:
At the first coagulation pattern, PT and APTT were significantly prolonged, and correction tests were conducted immediately, and the result was "can be corrected", indicating that the clinical patient's specimen lacked the possibility of related coagulation factors.
On the afternoon of January 30, the coagulation factor was sent for testing, the test result was 12% of the factor IX, so I contacted the patient's attending physician, and our analysis believed that the patient's 9 factor was low, and the PT prolongation was significantly higher than that of APTT, considering that it was mainly due to the lack of vitamin K-dependent coagulation factors (2, 7, 9, 10) caused by the prolongation of PT and APTT, and it was recommended to send out the relevant coagulation factors (our hospital did not carry out related coagulation factor testing).
On 2 February, given that the patient's PT test results were still around 40 seconds, combined with the fact that the patient was using a human prothrombin complex to supplement with factors 2, 7, 9, and 10 coagulation, it was recommended to add vitamin K1 again in clinical contact. PT was 14.8 seconds on February 4 and 11.8 seconds on February 6, and was discharged on February 6.
Two
Knowledge development
1. When the increase in PT is significantly greater than the increase in APTT, it often indicates the lack of coagulation factors FII, FVII, FIX, and FX, of which the half-life of FVII is the shortest. These coagulation factors require the participation of vitamin K in liver synthesis, so they are also called vitamin K-dependent factors.
2. Introduction of vitamin K
Vitamin K is a fat-soluble vitamin that needs to be absorbed by ileal epithelial cells and transported to the liver under the action of pancreatic enzymes and bile salts. When the liver synthesizes vitamin K-dependent coagulation factors, involved in the carboxylation reaction of glutamic acid, only γ-carboxy glutamate can bind to Ca2+ and connect them to the phospholipid surface by the Ca2+ bridge.
Naturally occurring VK1 is mainly found in leafy greens, and VK2 is synthesized from gut bacteria such as E. coli. Other synthetic VKs are water-soluble, such as K3, K4, etc.
3. Common causes of vitamin K deficiency:
Vitamin K deficiency is more common in infants and less common in adults and can be synthesized through food intake and intestinal flora.
Malabsorption: such as fasting patients or people with severe diarrhea.
Biliary tract diseases: lack of bile acids in the small intestine and impaired formation of microsomes, impaired absorption of fat-soluble vitamin K in food.
Liver disease: Even if vitamin K is not deficient, impaired liver function can lead to decreased synthesis of vitamin K-dependent factors. This is a vitamin K utilization disorder.
Long-term use of antibiotics:
Long-term use of antibiotics will have an inhibitory or killing effect on intestinal bacteria, affecting the synthesis of adequate amounts of VK in the normal intestinal flora.
In particular, the 3rd generation of cephalosporin is mainly metabolized by the biliary system, and E. coli in the intestine is very sensitive to such drugs. Cefoperazone sodium sulbactam sodium inhibits nearly 80% of E. coli, and this inhibition causes a significant reduction in vitamin K synthesis.
In addition, cefoperazone structure contains N-methylthiotetrazole, which is similar to the glutamic acid structure, and vitamin K is competitively bound to γ-glutamate carboxylase in the liver microsomals, making vitamin K-dependent coagulation factor production disorders, through the inhibition of vitamin K1 cyclooxide reductase, the vitamin K cycle in the body is blocked, and finally the reductive vitamin K deficiency involved in the activation of coagulation factors.
VK antagonists:
Such as oral warfarin or rat poisoning. Both belong to the coumarin class of drugs, which inhibit the activity of vitamin K epoxide reductase and thus block the production of reduced vitamin K, thereby inhibiting carboxylation of FII, FVII, FIX and FX.
Warfarin is the most commonly used anticoagulant in clinical practice. The second generation of double coumarin rodenticide, that is, anticoagulant rodenticide, is called "super warfarin", and the mechanism of action is similar to warfarin, but the efficacy is 100 times stronger than warfarin. The high lipophilicity of rat poison leads to slow excretion and a significantly longer half-life than warfarin, at least 16 to 69 days. Because coumarin drugs do not affect the coagulation factors that have been synthesized by the body, symptoms generally appear after oral warfarin overdose or contact with rat poison for several days, and it is necessary to pay attention to the recurrence of the course of the disease in people with rat poisoning.
Source: Department of Medical Laboratory, Affiliated Hospital of Nantong University
Edited by: Yeah Reviewer: Xiao Ran