CASE REPORT

                                  ABSTRACT
Current case is about an 80 y/o patient who has developed deep vein thrombosis as a consequence of organophosphate compound poisoning.

In this case, risk factors a/w development of DVT(without considering OP poisoning) is age (80 yrs) and comorbidity(hypertensive since 5 years)

                            INTRODUCTION


a case
a discussion
Some journals might require literature review.

CASE

80 year old female who is a homemaker came with complaints swelling in the left lower limb since 10 days associated with pain.
History of organophosphate compound poisoning 20days back for which she was treated outside and since then patient is on
 Tab. QUITIPINE 5R 500 OD, 
                    Tab. RISPERIDONE 2mg OD
  
K/c/o HTN since 5years on T
No similar complains in the past. 
Tubectomy done
No h/o any prolonged immobilisation. 


VITALS-
PR-80bpm
BP-130/80mmhg
RR-17cpm
SpO2-98% at RA
RS- BAE present
P/A-Soft and NT
CVS-S1S2 present
CNS-NFD


INVESTIGATION-
APTT-32sec
PT-16sec
INR-1.11


PROVISIONAL DIAGNOSIS-DVT OF LEFT LOWER LIMB. 

TREATMENT on day of admission-16/03/2021
1.INJ. CLEXANE 60mg SC OD. 
2.Monitor vitals. 
3. GRBS 12th hourly. 

TREATMENT ON DAY 1 -17/03/2021
S-
Subjectively patient is feeling better. 
C/o unilateral lower limb swelling of left leg. 
No skin induration. 
No change in appearance, colour. 
O-
Patient is c/c.
Afebrile
BP-140/80mmhg 
PR-78bpm normal volume and regular rhythm
CVS-S1 S2 present
RS-BAE present
PA-soft and NT
CNS-NFD
A-
LEFT LOWER LIMB DVT
P-
1.Inj. ENOXAPARIN 60mg SC OD. 
2.T. ATEN 50mg PO OD. 
3. T. QUITIPINE 5R500 PO OD. 
4. T. RISPERIDONE 2mg PO OD. 
5. T. DIMEFAS ODS 5mg PO OD. 

TREATMENT ON DAY 2-18/03/2021
S-
Subjectively patient is feeling better. 
No skin induration. 
No change in appearance, colour. 
O-
Patient is c/c.
Afebrile
BP-130/80mmhg 
PR-78bpm normal volume and regular rhythm
CVS-S1 S2 present
RS-BAE present
PA-soft and NT
CNS-NFD
A-
LEFT LOWER LIMB DVT. 
OBG referral was taken i/v/o any mass per vaginum-



P-
1.Inj. ENOXAPARIN 60mg SC OD. 
2.T. ATEN 50mg PO OD. 
3. T. QUITIPINE 5R500 PO OD. 
4. T. RISPERIDONE 2mg PO OD. 
5. T. DIMEFAS ODS 5mg PO OD. 

INVESTIGATIONS-
PT-18sec APTT-36sec INR-1.33

TREATMENT ON DAY 3-19/03/2021
S-
Subjectively patient is feeling better. 
No skin induration. 
No change in appearance, colour. 
O-
Patient is c/c.
Afebrile
BP-110/80mmhg 
PR-88bpm normal volume and regular rhythm
CVS-S1 S2 present
RS-BAE present
PA-soft and NT
CNS-NFD
A-
LEFT LOWER LIMB DVT
P-
1.Inj. ENOXAPARIN 60mg SC OD. 
2.T. ACITROM 2mg PO OD. 
3. T. QUITIPINE 5R500 PO OD. 
4. T. RISPERIDONE 2mg PO OD. 
5. T. ATEN 50mg PO OD. 

TREATMENT ON DAY 4-20/03/2021
S-
Subjectively patient is feeling better. 
No skin induration. 
No change in appearance, colour. 
O-
Patient is c/c.
Afebrile
BP-110/80mmhg 
PR-80bpm normal volume and regular rhythm
CVS-S1 S2 present
RS-BAE present
PA-soft and NT
CNS-NFD
A-
LEFT LOWER LIMB DVT
P-
1.Inj. ENOXAPARIN 60mg SC OD. 
2.T. ACITROM 2mg PO OD. 
3. T. QUITIPINE 5R500 PO OD. 
4. T. RISPERIDONE 2mg PO OD. 
5. T. ATEN 50mg PO OD. 

TREATMENT ON DAY 5-21/03/2021
S-
Subjectively patient is feeling better. 
No skin induration. 
No change in appearance, colour. 
O-
Patient is c/c.
Afebrile
BP-110/80mmhg 
PR-80bpm normal volume and regular rhythm
CVS-S1 S2 present
RS-BAE present
PA-soft and NT
CNS-NFD
A-
LEFT LOWER LIMB DVT
P-
1.T. ACITROM 2mg PO OD. 
2. T. QUITIPINE 5R500 PO OD. 
3. T. RISPERIDONE 2mg PO OD. 
4. T. ATEN 50mg PO OD. 
INVESTIGATIONS-
PT- 16sec APTT- 31sec INR-1.11



TREATMENT ON DAY 6-22/03/2021
S-
Subjectively patient is feeling better. 
No skin induration. 
No change in appearance, colour. 
O-
Patient is c/c.
Afebrile
BP-100/60mmhg 
PR-76bpm normal volume and regular rhythm
CVS-S1 S2 present
RS-BAE present
PA-soft and NT
CNS-NFD
A-
LEFT LOWER LIMB DVT
P-
1.T. ACITROM 2mg PO OD. 
2. T. QUITIPINE 5R500 PO OD. 
3. T. RISPERIDONE 2mg PO OD. 
4. T. ATEN 50mg PO OD. 



Cummulative incidence of deep vein thrombosis in patients with organophosphate poisoning and comparison patients.


Sample Participants
"We identified patients from the NHIRD who were hospitalized with OP poisoning (ICD-9 Code 989.3) for the first time between 2000 and 2011. The date of first hospitalization was used as the index date. For the OP poisoning cohort, we extracted 9223 patients with OP poisoning, including information on their age and sex, who had no history of DVT (ICD-9-CM 453.8) or PTE (ICD-9-CM 415.1, excluding ICD-9-CM 415.11) before the index date. Records indicating a history of DVT or PTE before the index date or those with incomplete age or sex information and missing variables were excluded from the control group. For each OP poisoning patient in the OP poisoning cohort, 4 controls without OP poisoning were randomly selected, frequency matched by sex, age (every 5-year span), and the year of the index date. A total of 9223 patients with OP poisoning and 36,892 people without OP poisoning were followed up until diagnosis of DVT or PTE, loss to follow-up, death, withdrawal from the insurance program, or the end of 2011, whichever occurred first."


Some studies have indicated that OP poisoning may increase lipid peroxidation, induce oxidative stress, and reduce glutathione levels. 
Under high oxidative stress, tissues may sustain damage and persistently exhibit an inflammatory response, leading to cellular necrosis.

Deep vein thrombosis (DVT) is the formation of blood clots predominantly in the deep veins of the legs. Severe DVT causes permanent damage to the leg. Pulmonary thromboembolism (PTE) is a potentially life-threatening disease involving pulmonary artery thrombosis or occlusion of the thrombotic occlusion system, and it can lead to the collapse of the respiratory or circulatory systems, resulting in death. Both DVT and PTE constitute venous thromboembolism which, when severe, carries a fatality rate of 11% to 30% within 30 days.

The triad of Virchow describes the 3 major risk factors that contribute to thrombosis, which are hypercoagulabililty, hemodynamic changes (stasis or turbulence), and endothelial injury or dysfunction.
Although OP intoxication is not a general risk factor for DVT or PTE, previous studies have shown that chronic inflammatory status is associated with coagulation abnormalities and increased risk of DVT and PTE.8 No study has investigated the association between OP intoxication and DVT or PTE. Therefore, we conducted a nationwide prospective cohort study that involved controlling for potential comorbidities to determine whether OP intoxication increases the risks of DVT and PTE.

https://journals.lww.com/md-journal/Fulltext/2015/01010/Increased_Risk_of_Deep_Vein_Thrombosis_and.17.aspx


OPs are lipophilic and may accumulate in various parts of tissues and organs after intoxication. OPs are subsequently released from these tissues into the bloodstream, and intoxication relapse may be prolonged, leading to various clinical manifestations.9 A recent report showed that OP intoxication may be associated with increased reactive oxygen species (ROS) production and lipid peroxidation.10 ROS may act as an initiator of cell apoptosis and organ lesions through various pathways. Under high oxidative stress, cells typically undergo necrosis as a result of tissue damage. Such tissue damage can include subchronic and chronic toxicity and biochemical and histopathologic changes in various tissues, such as those in the liver, kidneys, pancreas, vascular walls, and endometrium,11 as well as an intense inflammatory response.12 Inflammation may cause thrombotic tendencies and microvascular thrombosis by increasing procoagulant factors and inhibiting natural anticoagulant pathways.13 In addition, with chronic inflammatory response, the properties of the endothelium may become dysfunctional with multiple outcomes, including the loss of anticoagulant, antiaggregant, and vasodilatory properties.

Another acute phase reactant, C-reactive protein (CRP), is substantially altered during infection, trauma, surgery, and tissue necrosis, as well as in patients with burns, inflammatory disease, or advanced cancer.

Lee et al15 determined that serum CRP levels are highly correlated with the severity of acute OP intoxication but not with serum AChE levels. Therefore, CRP may be an effective alternative index for assessing the intoxication status of patients.

These mechanisms may explain why the patients with OP intoxication in this study exhibited significantly higher DVT and PTE rates, particularly in the presence of any comorbidity, compared with the control cohort.

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