Bimonthly assessment jan.

1) 26 year old woman with complaints of altered sensorium somce 1 day,headache since 8 days,fever and vomitings since 4 days.

a). What is the problem representation of this patient and what is the anatomical localization for her current problem based on the clinical findings?

Problem representation:

26 year old Immunocompromised lady presents with Acute onset Altered sensorium and signs of meningism.

Anatomical localisation:

In the background of immunocompromised State , length and tempo of the presentation I would think acute aetiology like infections, drugs and toxins.

With three years history of systematic lupus erythematosis where she was on methylprednisolone since three years leading to immuno suppression may flare up chances of infection. With detailed history the drugs which she was using like hydroxychloroquine , sulphasalazine,methylprednisolone, alandronic acid and gabapentin doesn’t explain her symptoms and on further probing the attenders at any point they refuse that she take poison or toxins

On the background of immuno suppression which symptoms like chronic headache fever neck pain loss of appetite Iwould think of infection which is involving her central nervous system likely result in altered sensorium and irrelevant talk.

On clinical examination Brudzinski and kernicks were negative though she had terminal neck rigidity and pain.  Fever chart seems to be stepladder suggestive of enteric fever  which is unlikely in this case as there are no features suggestive of enteric fever like pain abdomen vomitings loose tools etc

Considering the epidemiology i would list my differentials as tubercular meningitis, enteric fever, CNS lupus.

b) What is the etiology of the current problem and how would you as a member of the treating team arrive at a diagnosis? Please chart out the sequence of events timeline between the manifestations of each of her problems and current outcomes. 

Rare possibility that non-steroidal anti-inflammatory drugs like ibuprofen can cause meningitis in patients with lupus. The most plausible explanation for the association is a hypersensitivity reaction involving the meninges.  https://pmj.bmj.com/content/75/890/771

c) What is the efficacy of each of the drugs listed in her prior treatment plan that she was following since last two years before she stopped it two weeks back? 

Hydroxychloroquine : Both HCQ and Pl were well tolerated in the 48-week trial. There were no remissions. With the exception of the patient assessment of joint pain, all other joint measures were similar between the groups. Twenty-nine patients withdrew before the end of the trial although only 2 patients withdrew for adverse drug effects.

https://pubmed.ncbi.nlm.nih.gov/7983646/https://pubmed.ncbi.nlm.nih.gov/7983646/

Bisphosohonates for steroid induce osteoporosis : 

We included a total of 27 RCTs with 3075 participants in the review. Pooled analysis for incident vertebral fractures included 12 trials (1343 participants) with high‐certainty evidence and low risk of bias. In this analysis 46/597 (or 77 per 1000) people experienced new vertebral fractures in the control group compared with 31/746 (or 44 per 1000; range 27 to 70) in the bisphosphonate group; relative improvement of 43% (9% to 65% better) with bisphosphonates; absolute increased benefit of 2% fewer people sustaining fractures with bisphosphonates (5% fewer to 1% more); number needed to treat for an additional beneficial outcome (NNTB) was 31 (20 to 145) meaning that approximately 31 people would need to be treated with bisphosphonates to prevent new vertebral fractures in one person.There was high‐certainty evidence that bisphosphonates are beneficial in reducing the risk of vertebral fractures with data extending to 24 months of use. There was low‐certainty evidence that bisphosphonates may make little or no difference in preventing nonvertebral fractures.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6461188/

Oral corticosteroids: 

Forty-one patients (21 randomized to prednisone and 20 randomized to placebo) experienced a serologic flare. Analysis of severe flares occurring <or=90 days from randomization revealed that 6 occurred in patients taking placebo and none occurred in patients taking prednisone (P = 0.007). Severe flares resulted in an increase in the prednisone dosage to >40 mg/day and/or the addition of an immunosuppressive agent. Furthermore, improvement in scores on the Systemic Lupus Erythematosus Disease Activity Index, decreased levels of anti-dsDNA antibodies, and increased levels of C4 occurred 1 month after initiation of prednisone treatment.

https://pubmed.ncbi.nlm.nih.gov/17075807/

Sulphasalazine:

I couldn’t find good literature regarding efficacy of sulphasalazine in SLE.

 d) Please share any  reports around similar patients with SLE and TB meningitis?

cases of bacterial meningitis without initial CSF pleocytosis in adults have rarely been reported. Only 26 cases, including the present case, were found in a search of English abstracts in the MEDLINE database. Patients with documented neutropenia were excluded (Table 1) (6–20). Of these, 11 cases had Streptococcus pneumoniae, 10 had N meningitidis, two had Escherichia coli, one had Proteus mirabilis, one had Listeria monocytogenes and one had Haemophilus influenzae. Blood culture was performed in 24 cases and bacteremia was detected in 19. The outcome was documented in 20 cases. Seven patients died and two exhibited auditory disorders. The timing of antimicrobial therapy was analyzed in 18 patients. Empirical treatment had not been implemented in five patients. Neutropenia is known to be associated with no response in CSF (11). Lukes et al (21) reported that 45% of neutropenic patients with bacterial central nervous system infection did not have pleocytosis. Fishbein et al (8) also reported two other patients with neutropenia caused by bacterial meningitis with normal CSF cell counts. Therefore, we excluded patients with neutropenia from the literature review.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4211346/

e) What is the sensitivity and specificity of ANA in the diagnosis of SLE? 

Of 1010 ANA test results reviewed, 153 were positive. The group with positive ANA test results included more patients aged 65 years or older than the group with negative ANA test results (30% vs 15%, P < .003). The diagnosis of systemic lupus erythematosus (SLE) was established in 17 patients, all of whom had positive ANA test results. Other rheumatic diseases were found in an additional 22 patients. The estimated sensitivity and specificity of the ANA test for SLE were 100% and 86%, respectively. For other rheumatic diseases, sensitivity and specificity were 42% and 85%, respectively. The positive predictive value of the ANA test was 11% for SLE and 11% for other rheumatic diseases. Specificity and positive predictive value for ANA testing in the elderly patients were lower than among younger patients.The sensitivity of the ANA test for SLE was high, but overall the positive predictive value was low for SLE or other rheumatic diseases. Sensitivity was low for ANA testing among patients with non-SLE rheumatic disease. More selective test ordering might improve the clinical utility of this test. Clinicians ordering the ANA test should be aware of the test's low-positive predictive value in settings with a low prevalence of rheumatic disease, particularly among older patients.

https://pubmed.ncbi.nlm.nih.gov/8678710/

2) Please go through the two thesis presentations below and answer the questions below by also discussing them with 

2)https://youtu.be/jXVS5J1-RNE

What was the research question in the above thesis presentation? 

The research question 

1)will salt restricted diet decrease blood pressure?

2)can 24hr urinary sodium test reflect the amount of sodium consumed by an individual

What was the researcher's hypothesis?

Hypothesis is that, salt restriction doesn't effect blood pressure in all the individuals in the same way, and salt resistant individuals don't benefit from a restricted diet as much as a salt sensitive individual.

What is the current available evidence for the utility of monitoring salt excretion in the hypertensive population

The 24hr urinary sodium is a reflection of dietary sodium, and has better results than dietary recall method

https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-10/How-to-quantify-salt-intake-in-certain-patients

Daily salt intake based on 24-hour urinary sodium excretion (assuming that all sodium ingested was in the form of sodium chloride) with a formula: figure 2 shows a practical method to estimate salt or sodium intake.

Figure 2: Calculation for estimation of salt or sodium intake

Na (mg/day) = Na (mmol/day) x 23;  NaCl = Na (g/day) x 100/ 39,3

1 gram salt (NaCl) = 393,4 mg Na = 17,1 mmol Na

2b)https://youtu.be/sw8o8y5Yw_I

What was the research question in the above thesis presentation? 

The research question in the above thesis is whether magnesium plays a role in complications of diabetes mellitus 

What was the researcher's hypothesis? 

The researcher's hypothesis is that hypomagnesemia causes complications of dm2 irrespective of other confounding factors like age,duration of diabetes.

What is the current available evidence for magnesium deficiency leading to poorer outcomes in patients with diabetes? 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4938107/

In this retrospective study 673 diabetic patients were evaluated. 

According to Mg levels, the patients were divided into two groups; as normomagnesemic patients and hypomagnesemic patients.

There were 55 patients (8.2%) with diabetic retinopathy and 95 patients (14.1%) with diabetic neuropathy. Five hundred patients (74.3%)  had normoalbuminuria; 133 patients (19. 8%) had microalbuminuria (MA) and 40 patients (5.9%) had overt proteinuria. One hundred and seventy one patients (25.4%) had HbA1c levels equal or below 7%; and 502 patients (74.6%) had HbA1c levels above 7%. There was no statistical difference in age or duration of diabetes between the groups formed according to Mg levels. Although there were no differences between the groups for retinopathy and neuropathy, MA was more common in hypomagnesemic patients (p =0.004). HbA1c levels did not differ between the groups (p =0.243). However there was a weak negative correlation between serum Mg and HbA1c levels (r =-0.110, p =0.004) and also between serum Mg and urine protein level  (r =-0.127, p =0.018

3)Please critically appraise the full text article linked below:

https://onlinelibrary.wiley.com/doi/full/10.1111/j.1365-2796.2003.01233.x

What is the efficacy of aspirin in stroke in your assessment of the evidence provided in the article. Please go through the RCT CASP checklist here https://casp-uk.net/casp-tools-checklists/ and answer the questions mentioned in the checklist in relation to your article. 

Clinical appraisal of the article:

1)The study answered the research question 

being the use of asprin for prevention of stroke progression.

it was foccused in terms of intervention given and outcome measured

2)the method for randomisation was appropriate eliminating systematic bias and allocation sequence concealed from investigators and participants

3)all the participants included in the study were accounted for, including rhe two parcels whixh were accidentally opened.

4)the participants and the investigators were blind methodically

5)the study groups were similar 

6)apart from the experimentation, the hospital care given is not documented

7)there were dropouts in the study, study medication was interrupted in few due to suspected side effects,

the p value was not mentioned

8)the cI interval 95%0.6-1.45

9)the treatment effect wasn't much, 

10)the outcomes are benefial to my population in prescribing anticoagulants

dual vs single antiplatelet use and longer duration of followup could have been made .