IMMUNOLOGICAL BASIS OF GLAUCOMA

 

Experimental and clinical studies suggest a role of auto-immunity in the pathogenesis of glaucoma. A wide range of serum auto-antibodies especially against heat shock proteins (HSPs) and deposits of immunoglobins have been detected in glaucoma patients, as well as, animal models of glaucoma, pointing to an immunological mechanism for the causation of glaucoma.

It has been found that even transient intraocular pressure (IOP) elevation is sufficient to induce T-cell infiltration into the retina. This T-cell infiltration leads to a prolonged phase of retinal ganglion cell (RGC) degeneration that persists after IOP returns to a normal level.

A study found that inoculation of rats with human HSP27 and HSP60 induced an optic neuropathy that resembles glaucomatous neural damage, and elevated IOP has been reported to induce expression of HSPs in the retina, particularly in the RGCs. [1]

Therefore, an association of elevated IOP, HSP upregulation, and induction of anti-HSP autoimmune responses in glaucoma has been suggested.

A critical question is how autoimmune responses, such as those against HSPs, are induced in glaucoma? As HSPs are among the most highly conserved proteins from bacteria to mice to humans (up to 60% identity), a possibility is that the anti-HSP immune responses are induced originally by commensal bacterial HSPs, and are reactivated by host HSPs during glaucoma.

The fact that glaucoma patients exhibit increased titers of antibodies against Helicobacter pylori and that immunization with HSPs in rats induces glaucomatous neural damage are in line with this possibility. 

ALSO SEE THIS: https://ourgsc.blogspot.com/search?q=helicobacter

Both bacterial and human HSPs are target antigens of T cells; retina-infiltrating T cells cross-react with human and bacterial HSPs. HSP-specific CD4+ T-cell responses and glaucomatous neurodegeneration are both abolished in mice raised in the absence of commensal microbial flora (germ-free (GF) mice), supporting a mechanism of commensal microflora sensitized T-cell responses underlying the pathogenesis of glaucoma.

Chen et al, have hypothesized that mice harbor memory T cells to bacterial HSPs that can be activated by host HSPs through molecular mimicry when the blood-retinal barrier is compromised by elevated IOP. Their study indicates a need for prior exposure to commensal microbial flora in the induction of both HSP-specific T-cell responses as well as RGC and axon loss following IOP elevation. [1]

HSP-specific T-cell responses probably contribute to normal-tension glaucoma (NTG) as HSP immunization elicits glaucomatous RGC loss in rats. Elevation of IOP upregulates membrane-bound and extracellular HSPs in the ganglion cell layer of the retina, subsequently leading to immune-mediated neural damage through activating HSP-specific CD4+ T cells, which are originally induced by microbial HSPs.

REFERENCE:

[1] Chen H, Cho KS, Vu THK, Shen CH, Kaur M, Chen G, Mathew R, McHam ML, Fazelat A, Lashkari K, Au NPB, Tse JKY, Li Y, Yu H, Yang L, Stein-Streilein J, Ma CHE, Woolf CJ, Whary MT, Jager MJ, Fox JG, Chen J, Chen DF. Commensal microflora-induced T cell responses mediate progressive neurodegeneration in glaucoma. Nat Commun. 2018 Aug 10;9(1):3209. doi: 10.1038/s41467-018-05681-9. Erratum in: Nat Commun. 2018 Sep 20;9(1):3914. PMID: 30097565; PMCID: PMC6086830.

IOP rise in consensual eye after glaucoma surgery

 

A significant increase in IOP in the fellow eye (FE) after glaucoma surgery in the index eye (IE) has been noted by some researchers. Although, there are also reports of reduction in IOP in the FE after surgery in the IE.

See post on AMTT here: https://ourgsc.blogspot.com/search?q=AHMAD%27S

In a study performed on 187 consecutive glaucoma patients, who underwent either trabeculectomy or Ahmed Glaucoma Valve (AGV) implantation, it was found that nearly a third of them required medical or surgical management of IOP in the FE following surgery of the IE. [1]

In the study, 87.7% patients underwent trabeculectomy and 12.3% underwent AGV implantation.

Incidentally, in 84% of the patients the FE was already glaucomatous and 22 eyes had undergone trabeculectomy.

The mean IOP rise in FE among all patients (trabeculectomy and AGV), was as follows:

Pre-operative IOP in IE	17.6± 6.9 (n-187)
Pre-operative IOP in FE	14.48± 3.4 (n‑187)
IOP in FE: Post-op 1 day	14.54 ± 4.9 (p‑ 0.694)
Post-op 1 week	15.8 ± 5.5 (p‑0.005)
Post-op 1 month	15.62 ± 5.7 (p‑0.007)
Post-op 3 months	15.09 ± 5.0 (n‑135, p‑0.279)

 

Among patients with AGV shunt surgery (n=23), the mean fellow eye IOP was higher than baseline at all‑time points, with maximum rise on day 1 (15.91 ± 6.3, baseline 13.78 ± 2.7; n‑ 23, p‑0.066).

Pre‑operative acetazolamide (n=43) strongly predicted a statistically significant increase in FE mean IOP.

Among all patients, 15% required additional intervention to control IOP in the FE in the first 30 days and 33% in the first 90 days after glaucoma surgery in the IE.

In the trabeculectomy group, 35% patients required an increase in the anti-glaucoma medications or surgery in the FE, within 90 days of surgery in the IE.

In the AGV group, 18% patients required additional intervention in the FE within 90 days of surgery in the IE.

Among all patients, 14.4% eyes required surgical intervention in the FE.

Other studies have also noted a significant increase in IOP in the FE after glaucoma surgery. Meshksar reported maximum IOP rise 1 week after surgery [2], while Kaushik noted it at 6 weeks following surgery [3].

Incidentally, Kaushik did not report any significant association with acetazolamide.

A number of explanations have been surmised for this phenomenon. It is assumed that patients stop the anti-glaucoma medications in FE after surgery in one eye. 

Another potential explanation for the rise in IOP would be the sequelae of under-perfusion of the scleral meshwork due to preferential flow through the sclerostomy site. Under-perfusion results in meshwork densification, activation of endothelial cells and increase in extracellular matrix both in the ipsilateral and contralateral eye offering resistance to aqueous outflow and in turn contributing to the rise in consensual eye IOP. 

It has also been postulated that the scleral spur consists of special cells that play an important role in the afferent pathway of the reflex that controls bilateral ciliary body and meshwork contractile tone. Surgery in one eye could affect the other eye through these cells.

These studies indicate that close monitoring is required for the consensual eye after glaucoma surgery in one eye.

REFERENCE:

[1] Rajsrinivas D, Dubey S, Pegu J, Majumdar A. Consensual eye intra-ocular pressure rise following unilateral glaucoma surgery. Indian J Ophthalmol. 2023 Mar;71(3):873-879. doi: 10.4103/ijo.IJO_1909_22. PMID: 36872698; PMCID: PMC10230001.

[2] Meshksar A, Hajizadeh M, Sharifipour F, Yazdani S, Pakravan M, Kheiri B. Intraocular pressure changes in the contralateral eye after glaucoma surgery. J Glaucoma 2021;30:1074‑81.

[3] Kaushik S, Agarwal A, Kaur S, Lomi N, Raj S, Pandav SS. Change in intraocular pressure in the fellow eye after glaucoma surgery in 1 eye. J Glaucoma 2016;25:324–9.

SALIVA-BASED GENETIC TEST FOR GLAUCOMA

 

Researchers in Australia have devised a novel glaucoma polygenic risk score (PRS) that identifies those at high risk of losing their sight and prioritizes their treatment. The test performed on blood or saliva can detect the risk of glaucoma in 15-times more people, compared to other tests.

The lead researcher of the study, Associate Professor Owen Siggs, from the Flinders University, was quoted as saying that “Early diagnosis of glaucoma can lead to vision-saving treatment, and genetic information can potentially give us an edge in making early diagnoses, and better treatment decisions”. This can make genetic testing for glaucoma easier, and more commonly available early in the course of the disease.

The test is based on the premise that genetic variation is an increasingly powerful indicator in disease risk stratification. The study was performed to compare the polygenic and monogenic variants in risk of glaucoma.

The study involved 2507 individuals from the Australian and New Zealand Registry of Advanced Glaucoma (ANZRAG) and 411337 individuals in cross-sectional cohort studies including individuals of European ancestry in the UK Biobank.

The study reported that monogenic and high polygenic risk were each associated with a more than 2.5-fold increased odds of developing glaucoma and an equivalent mean age at glaucoma diagnosis, with high polygenic risk more than 15-times more common in the general population.

The saliva-based test will change the current one-size-fits-all approach to one of a more personalized approach where high-risk patients are managed with specialist input, while those at a low- and intermediate-risk level can be managed safely and less frequently in optometric primary care.

REFERENCE:

Siggs OM, Han X, Qassim A, Souzeau E, Kuruvilla S, Marshall HN, Mullany S, Mackey DA, Hewitt AW, Gharahkhani P, MacGregor S, Craig JE. Association of Monogenic and Polygenic Risk With the Prevalence of Open-Angle Glaucoma. JAMA Ophthalmol. 2021 Sep 1;139(9):1023-1028. doi: 10.1001/jamaophthalmol.2021.2440.

NLY01 in OCULAR HYPERTENSION

 

Astrocytes are a type of glial cell which form the majority of cells in the human central nervous system (CNS). In the retina they occur exclusively in the ganglion cell layer, mixed with retinal ganglion cells (RGCs).

In response to local or systemic stimuli, the astrocytes (A1 and A2) adopt reactive forms.

The A1 astrocytes develop pro-inflammatory and neurotoxic functions. They lose their phagocytic capacity, and their ability for synapse formation and function.

A2 astrocytes upregulate neurotrophic factors, promoting a neuroprotective environment.

ASTROCYTES IN GLAUCOMA

Sterling and associates have shown that ocular hypertension can trigger microglia to produce and release pro-inflammatory cytokines C1q, interleukin-1α (IL-1α), and tumor necrosis factor-α (TNF-α). These three cytokines are necessary and sufficient to drive the formation of A1 astrocytes.

Studies have demonstrated a strong association between the above mentioned three cytokines and glaucoma. IL-1α and TNF polymorphisms are associated with primary open angle glaucoma. TNF-α protein levels are elevated in the vitreous, retina, and optic nerves of glaucomatous eyes. In the DBA/2J mouse model of hypertensive glaucoma, C1qa mRNA levels are associated with disease progression, and C1q inhibition is sufficient to prevent early RGC synapse loss and RGC death.

Glucagon-like peptide-1 is an incretin hormone that regulates blood glucose, weight, and satiety through its action at the glucagon-like peptide-1 receptor (GLP-1R) in both the systemic circulation and the central nervous system. NLY01 is a long-acting GLP-1R agonist with an extended half-life and favorable blood brain barrier penetration.

Sterling has shown NLY01 therapy reduces the production of C1q, TNF-a, and IL-1a by the CD11b+ CD11c and CD11b+ CD11c+ dendritic cells in a mouse model of glaucoma. It also reduces A1 astrocyte transformation and RGC loss.

Therefore, NLY01 has potential clinical use in the treatment of glaucoma and possibly other retinal diseases characterized by reactive astrogliosis.

 

DEFERIPRONE IN GLAUCOMA MANAGEMENT

 

Currently, lowering of intra-ocular pressure (IOP) remains the main therapeutic option for the treatment of glaucoma. However, studies have shown that despite adequate control of IOP a large number of patients develop loss of visual function. This has spurred researchers to look for new options for the management of glaucoma.

According to Dr. Qui N. Cui, Assistant Professor of Ophthalmology at the Perelman School of Medicine, affiliated to the University of Pennsylvania, USA, “All available treatments for glaucoma target IOP control, which is not sufficient to prevent vision loss in a significant number of patients”.

Prof. Qui N. Cui

Apoptosis, pyroptosis, and necroptosis are classical forms of regulated cell death that play important roles in various diseases. Ferroptosis was a regulated cell death described by Dixon et al. who used elastin to treat cancer cells containing oncogene mutations. They found an iron-dependent and lipid peroxidation-triggered cell death pathway, which relies on iron-generated reactive oxygen species. In the eye, this process can lead to acute retinal degeneration.

There is increasing evidence supporting the association between ferroptosis and glaucoma. A clinical study involving 17,476 participants showed that a high serum ferritin level was associated with increased risk and morbidity of glaucoma. Upon facilitated release of ferric iron by increased ferritin, a redox reaction is triggered. This iron-induced oxidative stress is suggested to contribute to optic nerve degeneration in glaucoma. 

SEE LINK: https://ourgsc.blogspot.com/search?q=ferroptosis

Also, iron-related genes transferrin, ceruloplasmin and ferritin were shown to be upregulated in a monkey model of glaucoma, and in glaucomatous human post mortem eyes, suggesting a role for iron-induced oxidative stress in glaucoma pathogenesis.

Antioxidant administration has been shown to rescue rodent RGCs exposed to extended periods of IOP elevation. These associations suggest iron chelation may slow glaucoma progression.

Deferiprone (DFP), is an orally-administrated iron chelator approved by the FDA for treating patients with iron overload. Oral administration of DFP protects against iron-induced retinal degeneration by reducing retinal iron levels in ceruloplasmin/hephaestin double-knockout and hepcidin knockout mice, both of which exhibit age-related retinal iron accumulation and increased oxidative stress.

In a study performed by Dr. Qui and colleagues, a mouse model of elevated IOP was used in which one eye had experimental ocular hypertension and the other was kept as normotensive control. Half the cohort received oral DFP (1 mg/ml in the drinking water), the other half did not and served as controls. After 8 weeks, Brn3a immunolabeling of flat-mounted retinas was used for manual RGC quantification. Axon counts were obtained from thin sections of optic nerves using the AxonJ plugin for ImageJ.

DFP administration was found to be protective against RGC and optic nerve loss in the setting of elevated IOP. These results suggest that iron chelation by DFP may provide glaucoma neuroprotection.

A side-effect of DFP administration is reversible agranulocytosis, which requires weekly blood evaluations. Therefore, the utility of DFP as long-term treatment for a slowly progressive neurodegenerative condition like glaucoma remains to be seen. Alternatives to systemic DFP administration may lie in local, targeted ocular administration and/or other iron chelators.

REFERENCE:

Cui QN, Bargoud AR, Ross AG, Song Y, Dunaief JL. Oral administration of the iron chelator deferiprone protects against loss of retinal ganglion cells in a mouse model of glaucoma. Exp Eye Res. 2020 Apr;193:107961. doi: 10.1016/j.exer.2020.107961. Epub 2020 Feb 8. PMID: 32045598; PMCID: PMC7584350

Dixon SJ, Lemberg KM, Lamprecht MR, Skouta R, Zaitsev EM, Gleason CE, Patel DN, Bauer AJ, Cantley AM, Yang WS, Morrison B 3rd, Stockwell BR. Ferroptosis: an iron-dependent form of nonapoptotic cell death. Cell. 2012 May 25;149(5):1060-72. doi: 10.1016/j.cell.2012.03.042. PMID: 22632970; PMCID: PMC3367386.

HELICOBACTER PYLORI ASSOCIATED GLAUCOMA

Helicobacter pylori (H. pylori) is a spiral-shaped and gram-negative micro-organism that affects the epithelial mucosa of the stomach. In that site it usually causes peptic ulcer, gastritis and cancer.

Ocular manifestations of H. pylori infection include glaucoma, central serous chorioretinopathy (CSR), blepharitis, and uveitis.

It is presumed that H. pylori causes glaucoma by various mechanisms, including the release of various pro-inflammatory and vasoactive substances such as reactive oxygen species, through arteriosclerosis-induced increased platelet activation and aggregation, and impact on the trabecular meshwork cell apoptotic process.

H. pylori infection is also responsible for induction of oxidative DNA.

Cross-reactivity between antibodies to H. pylori and the ciliary epithelium and antibody-induced apoptosis has also been speculated.

Glaucoma patients have a common genetic factor that makes them more susceptible to H. pylori infection.

A meta-analysis involving 24 studies was performed to look into the probable association of H. pylori with glaucoma. Out of those 7 were cohort and 17 case-control studies. [1] 

This meta-analysis showed a statistically significant relationship between H. pylori infection and glaucoma, and further analysis showed that this positive relationship is observed in primary open-angle glaucoma (POAG), normal tension glaucoma (NTG) and pseudo-exfoliative glaucoma (PXG).

In studies by Shahram Ala et al., and also by Kountouras, H. pylori eradication treatment positively affected glaucoma management. The results showed that intraocular pressure decreased significantly after eradication treatment in the intervention group. [2] [3]

These studies suggest that this cause can be considered in certain areas where H. pylori infection is endemic.

REFERENCES:

1. Ezzati Amini E, Moradi Y. Association between helicobacter pylori infection and primary open-angle glaucoma: a systematic review and meta-analysis. BMC Ophthalmol. 2023 Sep 11;23(1):374. doi: 10.1186/s12886-023-03111-z. PMID: 37697285; PMCID: PMC10496366.

2. Ala S, Maleki I, Araghi AS, Sahebnasagh A, Shahraki A. Helicobacter pylori eradication in the management of glaucoma. Caspian J Intern Med. 2020;11(2):143.

3. Kountouras J, Mylopoulos N, Chatzopoulos D, Zavos C, Boura P, Konstas AG, Venizelos J. Eradication of Helicobacter pylori may be beneficial in the management of chronic open-angle glaucoma. Arch Intern Med. 2002;162(11):1237–44

LOW VISION AIDS IN GLAUCOMA

 

Glaucoma is characterized by classical visual field loss patterns. In early glaucoma there is mainly restriction of the peripheral fields. But in later stages central vision is also impaired, affecting the quality of life of the glaucoma patient. However, there are some studies which have shown that even central vison can be affected early in the course of glaucoma. As visual deterioration develops, there occurs a situation in which usual visual rehabilitation methods such as glasses become ineffective. In such cases low vision aids (LVA) may prove helpful.

Overall, visual rehabilitative services include mobility training, adaptive skills training, low vision instruction career services and training, psychological counseling and others.

Some other useful links:

How to break bad news: https://ourgsc.blogspot.com/search?updated-max=2024-04-13T12:52:00%2B05:30&max-results=1&start=1&by-date=false

SPIKES protocol: https://ourgsc.blogspot.com/search?updated-max=2024-04-16T09:24:00%2B05:30&max-results=1&reverse-paginate=true

Low vision aids are devices which help people use their sight to better advantage. These aids fall into two categories, namely, optical and non-optical. The former includes optical lenses, such as magnifiers or telescopes. The non-optical devices include visors, filters, reading slits, stands, lamps and large print. The basic principle of all low vision optical devices is to magnify.

OPTICAL DEVICES:

1. Magnifying spectacles (high plus reading glasses) used for reading any material, writing and looking at objects from close range. The spectacle produces magnification of 1/4th of the power of the lens. For binocular corrections prism spectacles half eyed of full field with base in (to compensate for convergence angle of the eye) are used.

2. Magnifiers: Handheld low vision magnifiers are helpful for looking in a mirror, telling the time on a watch, and other quick viewing tasks. The ones with self-contained illumination can be used when surrounding illumination is dim. The low vision magnifiers that are mounted on a stand are useful for reading books and doing close-up work such as needlepoint and quilting.

3. Telescopes: These are prescribed for distance, near and intermediate tasks like reading signs, recognizing people, reading from blackboard at more than 2-meters distance, watching television, games or traffic signals. These can be hand held monocular, clip on, spectacle mounted, monocular or binocular, bioptic designs.

4. E-Scoop glasses: E-Scoop Glasses are custom designed optics that combine 5 unique optical characteristics to maximize the remaining vision of a low vision patient. These 5 optical features focus the image onto the part of the eye that is least affected by vision loss, thereby maximizing the patient’s current vision.

5. Envision glasses: Envision Glasses are AI-powered smart-glasses with an integrated camera and built-in speakers that speak out the visual world. It is a wearable device that significantly improves the daily life of people that are blind or have low vision. It provides an intuitive and easy way to access all kinds of visual information around them. 

6. IrisVision: These electronic glasses use a highly innovative assistive technology solution, which is registered with the FDA as a Class-1 medical device.

7. Acesight: It is a wearable LVA is based on ‘Augmented Reality’ technology. It offers an HD display floating before the eyes, through a pair of head-mounted goggles, which are connected to a controller through a wire. It provides up to 15X magnification, while the wired controller allows one to customize the colors and contrast. This electronic eyewear is designed to cater to the needs of people with visual acuity ranging from 20/100 to 20/800.

8. NuEyes Pro: It is a head-worn lightweight and wireless pair of smart glasses, which can be controlled either through a wireless handheld controller or a set of voice commands. A camera on the front of the glasses captures the image and displays it magnified inside of the lenses. These glasses provide up to 12X magnified images.

9. MyEye2: These are low vision electronic glasses designed to make reading, writing, recognizing faces and various other daily activities easier for visually impaired people. A light attachable camera distinguishes it from an ordinary pair of glasses, which is mounted on the frame of the glasses by the side.

NON-OPTICAL DEVICES:

1. Typoscopes are used to enhance images and reduce glare. Felt tipped pens, bold lined papers, writing guide, large print materials and adequate lighting on print are helpful methods in assisting vision by enhancing contrast. Reading stands are useful by providing a hands-free comfortable working distance.

2. Assistive Technologies: Desktop electronic magnifiers are low vision aids that display reading material placed on a tray. The person with low vision moves the reading material as needed and views it on a screen at a suitable height. Most of these magnifiers have an independent monitor, but others allow for connection to a TV or computer monitor. Often these devices are a bit heavy and therefore are not portable. There are portable low vision electronic magnifiers, which are of two main types. The handheld ones can be carried in a pocket or handbag, and are used to read labels in a grocery store or pharmacy, menus in a restaurant, credit card slips, price tags and more. The other type has a camera fixed to a stand. Therefore, a still image of the reading material can be taken and can be read later on a portable device.

Supernova magnifier

Juno Magnifier

LIMITATION: The non-availability of trained personnel as well as the financial cost and practicality of the LVAs remains a limitation for their usage in glaucoma clinics.

CARONIA GLAUCOMA CARD

 

The Amsler Grid chart, a commonly used method for detection of macular pathologies, has been utilized in detection of visual field (VF) defects in advanced glaucoma. [1]

However, a new card developed by Dr. Ronald Caronia, is apparently more efficacious in detecting scotomas and readily acceptable by patients with severe glaucoma compared to the Amsler grid. [2]

The Caronia Glaucoma Card (CGC) design incorporates a vertical and horizontal line and seven concentric circles corresponding to 1-degree arc at normal reading distance.

The 7 concentric circles surround a central ‘X’. The first circle surrounding the ‘X’ creates 1-degree of arc from the center, and each of the other circles creates an additional 1-degree arc from the previous circle.

The end result is a card which evaluates 7 degrees of peripheral field from fixation, giving the full extent of peripheral field testing to 14 degrees.

In a study conducted by Dr. Caronia, the patients were given a card on which the Amsler grid was printed on one side and the CGC on the other. The patients were asked to use either one or both tests to monitor their visual function on a weekly basis. Upon return, they were asked which test they preferred and if they appreciated or noticed any change in their scotoma.

The study reported that 30 patients out of 67 preferred the CGC (60%), while 8 patients preferred the Amsler grid (16%) for monitoring their VFs. Twelve patients found no difference between the 2 test designs (24%). [χ² (2, 50) =16.480, ρ=0.000]. Five patients noticed a change in their scotoma while using the card (5.8%, 5 of 86 eyes). All were exclusively using the CGC.

The report concluded that the CGC is a convenient and inexpensive tool to assess VF defects in glaucoma and has high acceptance by patients to monitor their glaucoma status.

REFERENCES:

1. Gessesse GW, Tamrat L, Damji KF (2020) Amsler grid test for detection of advanced glaucoma in Ethiopia. PLoS ONE 15(3): e0230017. https://doi.org/10.1371/journal.pone.0230017

2. Caronia RM. Caronia Glaucoma Card Versus Amsler Grid for Monitoring Patients With Advanced Glaucoma. J Glaucoma. 2024 Apr 1;33(4):277-287. doi: 10.1097/IJG.0000000000002336. Epub 2023 Nov 24. PMID: 38031281.

SPIKES Protocol

 

The SPIKES Protocol is a common template for breaking bad news for different morbid conditions, especially cancer. For the ophthalmologist, this can come handy in dealing with glaucoma patients.

The acronym SPIKES, stands for Setting up, Perception, Invitation, Knowledge, Emotions with Empathy, and Strategy or Summary.

It is helpful to be reminded that, although bad news may be very sad for the patients, the information may be important in allowing them to plan for the future.

S- SETTING UP:

An appropriate setting with as much privacy as possible is required to establish rapport with the patient and/or family. Any disturbing influences such as phones, TV or radio should be turned off. The HCP should ensure that there are no distractions from other staff members. Setting the stage for optimal communication by preparing what to say prior to the conversation is essential to successful communication. The rules of preferred body language for optimal communication including sitting while speaking, maintaining an open posture, and maintaining eye contact apply as the interview environment is considered.

P- PERCEPTION:

The HCP should obtain all relevant information, including medical facts regarding the patient’s condition prior to conducting the interview. It is better to follow the “before you tell, ask” axiom, and ask open-ended questions initially so as to get some idea about the patient’s understanding of the condition. Subsequently, the HCP can correct any misinformation and explain the situation to the patient, especially with regards to the irreversible loss of vision which has already occurred and the expectations for the future. But most importantly the HCP should be in a position to understand the feelings of the patient/family and direct them towards a more honest understanding of the situation. The challenge for all clinicians is to respect the level of information desired, but have the patient and family know enough so that they are able to provide informed consent for further testing and treatment.

I- OBTAINING THE PATIENT’S INVITATION FOR DISCUSSION:

Every person has a different coping mechanism for their illness. A majority might be interested in knowing the problem, why they developed glaucoma, if there are any ways to prevent further visual loss and the types of treatments available. Others do not wish to know the details and inform the HCP that they have faith in their management and would leave all those aspects for the doctor. If the patient does not want to know the detailed results, one must offer to address any queries that they may have in the future, once their mind is at ease, or provide the details with subsequent implications to a care provider or family/friend.

K- GIVING KNOWLEDGE AND INFORMATION TO THE PATIENT:

The first step in actually delivering the news is to “Fire a Warning Shot” and warn the patient and family that the incoming news is not good.

The sharing of bad news must be presented based on the assessed level of patient’s understanding, compliance, and wishes for disclosure. Instead of using technical language regarding tests such as visual fields or OCT, the HCP can devote more time on the basic aspects of glaucoma and how the condition is affecting his visual pathway and what treatment is doing to his condition. The actual sharing of the bad news should be done slowly so that the patient and family understand. Appropriate words, especially in a stage of diverse cultural pool, have to be carefully chosen.

E- ADDRESSING THE PATIENT’S EMOTIONS WITH EMPATHIC RESPONSES:

Responding to the patient’s emotions is one of the most difficult challenges of breaking bad news. Patients’ emotional reactions may vary from silence to disbelief, crying, denial, or anger. This creates a potentially awkward situation for the HCP, but this sense of awkwardness can be diminished through engaging in empathetic communication.

In cases of advanced glaucoma with a risk of snuff-out, the visual prognosis is poor. However, the doctor must avoid using phrases such as total blindness, and rather focus on revised therapeutic goals and expectations.

S- STRATEGY AND SUMMARY:

The main aim of the interview is to present a clear plan or strategy for the patient, keeping in view the patient’s perception of the condition and the prognosis. Studies have shown that patients who have a clear plan for the future are less likely to feel anxious and uncertain. The future management plan should be discussed by the HCP. This is legally binding in some situations.

Sharing responsibility for decision-making with the patient may also reduce any sense of failure on the part of the physician when treatment is not successful. The doctor must check that the patient does not misunderstand the efficacy or purpose of the treatment, e.g., that the vision loss or visual field loss that has already occurred will not be restored by any subsequent intervention. In glaucoma patients the idea that the vision could improve after surgery or laser has to be cleared.

Finally, the HCP can re-cap a summary of the discussion in order to reinforce the ideas discussed with the patient.

STRATEGIES FOR BREAKING BAD NEWS

 

A delicate situation encountered by physicians is when they are called to break negative or bad news regarding the disease to the patients and/or their families. “Bad news” may be defined as “any information which adversely and seriously affects an individual’s view of his or her future”.

For a healthcare-provider (HCP) treating glaucoma, this situation can occur during the initial consultations itself, when the visual prognosis is poor or guarded. Often, the patients consult an ophthalmologist when they are already in the advanced stage of the disease, in the hope of recovering their vision. While others, follow a path of slow deterioration, losing a major part of their visual field over time, despite adequate treatment by the ophthalmologist. 

For a HCP, good communication skills are an integral part of high-quality patient care. To be able to effectively convey bad news can be a significant factor in improving the quality of life of the patient.

Breaking bad news involves a twofold process of finding appropriate kind words and understandable terminology, and the secondary task of assessing how the patient and family are reacting, the degree of distress that the conversation is inducing, and the subsequent tailoring of information as the HCP responds to the assessment process. The last segment of this communication is to move the patient and family from the bad news to the future plans with realism and hopefulness.

In order of simplify the process of breaking bad news a few strategies are being used. These include the SPIKE, BREAKS and ABCDE protocols. The acronyms stand for SPIKE (Setting, Perception, Information, Knowledge, Emotions & empathy, Support), BREAKS (Background, Rapport, Explore, Announce, Kindling and Summarize), ABCDE (Advance preparation, Building therapeutic relationship, Communication, Dealing with patient/family, Encouraging emotional responses/outbursts & offering solutions).

The SPIKES strategy/protocol was designed by Walter Baile and colleagues at the University of Texas MD Anderson Cancer Center in USA, and is designed to offer HCPs an effective mechanism to break bad news. The protocol focuses on the following steps:

1. Establishing an appropriate setting.
2. Checking the patient’s perception of the situation prompting the news regarding the illness or test results. 
3. Determining the amount of information known or how much information is desired. 
4. Knowledge of the medical facts and their implication before initiating the conversation.
5. Exploring the emotions raised during the interview and responding with empathy. 
6. Establishing a strategy for support.

Subsequent posts on The Glog shall present in detail the features of the SPIKES strategy.