A 60 yr old housewife with h/o Hypocalcemia, Hypokalemia and renal stone complaining of developing nearsightedness

 

NOTE: THIS IS AN ONLINE E LOGBOOK TO DISCUSS OUR PATIENT'S DE-IDENTIFIED HEALTH DATA SHARED AFTER TAKING HIS / HER /GUARDIAN'S SIGNED INFORMED CONSENT. HERE WE DISCUSS OUR INDIVIDUAL PATIENT'S PROBLEMS THROUGH A SERIES OF INPUTS FROM THE AVAILABLE GLOBAL ONLINE COMMUNITY OF EXPERTS INTENDING TO SOLVE THOSE CLINICAL PROBLEMS WITH COLLECTIVE CURRENT BEST EVIDENCE-BASED INPUT

PATIENT'S HISTORY: The patient is a 60-year-old housewife. In 2013, she had an episode of probable stroke followed by nausea, vomiting, diarrhea, weakness, fatigue with loss of appetite, and insomnia. Her legs felt numb. She lost sensation around neck. Had to be admitted to a nursing home. Diagnosis of hypocalcemia and hypokalemia was made. Got discharged after 5 days when k+ and Ca2+ lvl. returned to normal via i.v infusion. For 2 yrs she was fine. In 2015,  due to diarrhea and fatigue she got admitted to a Nursing home and stayed there for 7 days. Ca2+ and K+ lvl. was falling, so restored via i.v infusion. This time hypernatremia was also detected. Discharged after her conditions improved. But 2 days later, again due to severe diarrhea had to be admitted to a Nursing home for 19 days. During her stay USG of abdomen, colposcopy and chest X-ray was done. USG detected a large renal calculus measuring 22mm in rt. kidney. Sx was recommended. Pt went to Bhopal for a second opinion 

Previous case report done by an elective student 2015 - http://globaludhc07.blogspot.com/2015/12/a-50-years-old-woman-with.html?m=1

Clinician advised against surgery because she was not in pain. Her TSH is normal. A CT abdomen revealed a left adrenal cortical tumor. Diagnosis of pri. aldosteronism was made. Patient is hypertensive since 1995 since her second childbirth. Now BP is normal with medication. She is nondiabetic. Pt. advised to report her Ca2+ and K+ lvl. monthly. Pt.  acq. the habit of eating paan (beetle leaf) from her mother in 2011 when she came to stay with her. Used to eat 3-4 paans a day. Stopped in 2013 after Dr. advised against it.

                                       

CURRENT CHIEF PROBLEMS  AND PATIENT'S REQ.: 14 days ago, when making lemon juice, some of it went in her rt. eyes. Due to irritation and burning sensation, also inability to see far objects clearly(nearsightedness) with rt. eye she consulted an ophthalmologist, who diagnosed her to be having cataract in her rt. eye. Eye drops were given. A few days later she went again for an eye check-up and optic nerve atrophy possibly due to? glaucoma detected. Using the eyedrop gives relief, but she sometimes feels a burning sensation in her rt. eyes. She wants a second opinion about her eye condition. 

FAMILY HISTORY : 

Father - died at the age of 57 due to a stroke. Was a pt. of HTN

Mother - low pressure. 

Husband - Diabetic and HTN for the past 3 yrs. Now in control with medication. Hyperuricemia leading to jt. pain

Both daughters suffer from hypothyroidism

CURRENT MEDICATION - 

Aldactone 100

Shelcal 500 (dosage reduced to q.d)

Latoprost rt eye drop

REPORTS:

         Right eye(OD)

      Left eye(OS)

 Hematology report

Troponin I test - negative

2015

2015

2013

2013

2015

2015

PTH - within normal range 64 pg/ml

Urine report 2015

http://globaludhc07.blogspot.com/2015/12/a-50-years-old-woman-with.html?m=1 

CASE DISCUSSION:

[5:16 pm, 13/06/2022]  Sir, I went through the reports.

The suspected Glaucoma, d/t Optic nerve atrophy might have indicated Timolo

[5:16 pm, 13/06/2022]  Also the Opthalmologist have said it to be POAG ( primary open angle glaucoma)

[5:16 pm, 13/06/2022]  But the pressure findings ain’t there.

[5:16 pm, 13/06/2022]  Yes. What happened to those findings

[5:16 pm, 13/06/2022]  I think IOP was not considered for Dx or Rx of Glaucoma Sir.

The Dx was Open Angle Glaucoma based on Retinal findings. A/c the the drugs to decreas IOP was given?

[5:16 pm, 13/06/2022]  Excellent! So how are drugs used to reduce pressure useful in open angle glaucoma?

[5:16 pm, 13/06/2022]  Sir ,

Recently i had written a review on Glaucoma treatment trends .

So while studying i found we don’t exactly know the etiology behind Glaucoma.

There’s this increased IOP as the most accepted hypothesis.

Which is considered as the mainstream for Rx of Glaucoma.

Reducing the IOP is the 1st line target 🥲

[5:16 pm, 13/06/2022]  Exactly the reason for my interest in this topic

[5:16 pm, 13/06/2022]  Without reading your review please see if you have any answers to the questions below (with more fresh review of literature if feasible) :

What is the morphologic basis for diagnosis of normal pressure glaucomas? 

Can we start IOP reducing therapies in normal pressure glaucomas? What are the RCT efficacies of such pressure reducing therapies in normal pressure or open angle glaucomas?

Also to this Sir,

HTN induced can be ruled out.

As in the Retinal Examination, we didn’t see neovascuLarisation.

This should be seen before it is induced by HTN .

Plus hemmorhagic spots too

https://eyewiki.aao.org/Normal_Tension_Glaucoma

[5:51 pm, 13/06/2022] : The role of IOP in the pathogenesis of NTG is an area of controversy prompting research into a variety of IOP independent factors such as vascular dysregulation, hypotension, and lamina cribrosa abnormalities that may have some role to play in the development of this disease. Therefore, other proposed interventions in NTG have aimed at modification of blood pressure and optic nerve perfusion in addition to neuroprotection as a means of slowing disease progression independent of an IOP lowering mechanism. Despite the lack of an observed IOP elevation, the current medical and surgical treatment of NTG continues to be aimed at lowering IOP as in other forms of POAG.

[5:51 pm, 13/06/2022] Yes. Exactly why do we continue to use IOP lowering therapies knowing very well that IOP is not the target? 

Unless there are efficacy studies in IOP lowering therapies vs placebo in NTG (normal tension glaucoma?

[5:51 pm, 13/06/2022]  The Collaborative Normal Tension Glaucoma Study (CNTGS) demonstrated the benefit of IOP reduction for the treatment of patients with NTG[18][19]. The study concluded that a 30 percent reduction in baseline IOP resulted in a reduced risk of disease progression. Criteria for initiation of treatment of the NTG patients in this study were defined as: documented visual field or optic nerve progression, visual field loss threatening fixation, or presence of disc hemorrhage. The treatment group had a 12% risk of progression at 5 years compared to 35% progressing in the non-treatment group[19]. The CNTGS trial was therefore instrumental in demonstrating the role of IOP in the pathogenesis of NTG and the benefit of treatment to lower it. The study also presents a reasonable goal for treatment in 30% IOP reduction from patient’s baseline. Treatment IOP goals may then be modified over the course of treatment to a level that sufficiently prevents or slows progression of disease.

Outside of IOP lowering therapy, other aspects should be considered in the management of NTG patients. This may include cardiovascular problems such as systemic hypotension, nocturnal hypotension, anemia, and cardiac arrhythmias that can compromise optic nerve head perfusion. Consultation with primary care physicians can be helpful in addressing these concerns, but limited evidence is available to confirm a treatment benefit for NTG.

[5:51 pm, 13/06/2022]  Particularly with NTG, the effect of medications on systemic blood pressure, heart rate, and optic nerve perfusion should be considered. Furthermore, medications that have neuroprotective or IOP independent effects would be extremely beneficial and remain an ongoing search. The Low-Pressure Glaucoma Study (LoGTS) demonstrated the importance of IOP independent factors when choosing medical therapy for NTG[27]. In this prospective trial, patients with low-tension glaucoma were randomized to treatment with either brimonidine tartrate 0.2% or timolol maleate 0.5%. While IOP reduction was similar between the two treatment groups, patients treated with brimonidine were less likely to have visual field progression compared to patients treated with timolol. It is unclear whether this difference is due to an additional neuroprotective effect of brimonidine or a detrimental vascular effect from timolol. Moreover, Rho-kinase inhibitors are thought to be neuroprotective and increase vascular flow at the ONH via the nitric oxide pathway [65] [66]. Further trials are needed to identify ideal medical therapy in patients with NTG.

[5:51 pm, 13/06/2022]  Prognosis

Like any form of glaucoma, NTG may progress to irreversible blindness. The prognosis for visual preservation is good in patients who undergo adequate treatment through IOP reduction. In the CNTGS trial, 65% of patients in the control group with NTG did not progress even without treatment[19]. However an IOP reduction of 30% with treatment further lowered the likelihood of progression to only 12%. As mentioned previously, patients with NTG that previously suffered an acute vascular compromise have also been shown to not progress over time as well. Given this relatively high rate of non-progression, some clinicians have suggested a conservative “wait and see” approach to initiating treatment. This recommendation should be cautioned, as it is often difficult to determine which patients will progress, and other studies have shown variable rates of progression in this disease. Risk factors for progression of visual field defects in NTG include migraine, disc hemorrhage, and female gender. Asians have been shown to have a slower rate of progression[41].