A 65-Year-Old Man With Hypertension, COPD, Type 2 Diabetes, Headaches, Tinnitus, Symptoms of Erythromelalgia
This podcast series aims to highlight the prevention, diagnosis, and treatment of patients with diseases commonly seen in internal medicine. Host, Anil Harrison, MD, discusses patient cases with residents and with prominent experts to help educate clinicians in treating patients using a multidisciplinary approach.
In this episode, Dr Harrison discusses a case presentation of a 65-year-old man with chronic obstructive pulmonary disease, hypertension, and type 2 diabetes, who presents with headaches and bilateral tinnitus for 6 months. The patient describes the headaches as generalized, continuous, and mild, without any constitutional symptoms or fever. He also reports symptoms of erythromelalgia.
TRANSCRIPTION:
Jessica Bard:
Hello everyone and welcome to Multidisciplinary Dialogue Clinical Rounds and case reviews with your host Dr Anil Harrison, who is the program director and chair of the Internal Medicine Residency Program at the University of Central Florida and HCA Florida West Hospital in Pensacola, Florida. Dr Harrison has prepared a Grand Rounds episode for us today. The views of the speakers are their own and do not reflect the views of their respective institutions or the views of Consultant360.
Hello, Dr. Harrison. How are you this morning?
Dr Anil Harrison:
Good morning, Jessica. I'm doing very well, thank you.
Jessica Bard:
I am happy to hear that. We have an interesting patient case presentation, and we’d like to hear your thoughts on how to care for this patient. Please tell us about our patient today.
Dr Anil Harrison:
It's an interesting patient, I would say, Jessica. We have a 65-year-old hypertensive with COPD and type two diabetes mellitus who presents with headaches and bilateral tinnitus for six months.
The headaches described are generalized, continuous, mild, though nagging, without any constitutional symptoms, nor fever. He also reports symptoms of erythromelalgia. You mention the patient's blood pressure is 150 over 94. His heart rate is 80 per minute. His temperature is 98 degrees Fahrenheit, his respiratory rate is 14, and his BMI is 35. In his personal history, he smokes and consumes a couple of martinis every day, shaken, not stirred. He lives with his sixth wife, 30 years of age, who happens to be a pastry chef, he lives at 10,000 feet altitude in Mount Taos and is an avid YouTuber, who is living a life of splendor.
His medications include maximum doses of chlorthalidone, lisinopril, amlodipine, canagliflozin, a long-acting muscarinic agent inhaler, a long-acting beta agonist inhaler, and a short-acting rescue inhaler. His exam reveals mildly erythromelaticis bombs, and a few wheezes on auscultation. His cardiovascular, central nervous system and abdomen systems are benign. Jessica, the synopsis is we have a male in his mid-60s with hypertension, type two diabetes, and COPD who presents with chronic persistent headaches associated with bilateral tinnitus and erythromelalgia. The labs that you've shared reveal an H/H of 16.5 and 49, a white cell count of 5,000, and a platelet count of 210,000.
His sodium is 140, his potassium is 3.4, his chloride is 100, and his bicarb is 27. His BUN is 20, his creatinine is 1.5. His PSA is 4.2. His hemoglobin A1C is 7.8. On his lipid panel, his total cholesterol is 210. His LDL cholesterol is 112, his HDL is 37, and his triglycerides are 400 milligram percent. His testosterone levels are 150 and he had a stool guaiac times one, which is negative, and he is up-to-date on his immunizations until 20 years ago. If you realize one thing, Jessica, our minds have an uncanny way of picking things that are out of sorts.
With our patient, the H/H of 16.5 and 49, along with a potassium of 3.4, a creatinine of 1.5, a PSA of 4.2, and perhaps a hemoglobin A1C of 7.8, total cholesterol of 210, an LDL of 112, HDL of 37 and triglycerides of 400 along with a testosterone level of 150, to me, seem abnormal. I also wonder why only one stool guaiac was done, because there is nothing in history to suggest we are looking for an occult GI bleed. Although if this were for colon cancer screening, we know that one specimen is not enough, one needs three consecutive stool guaiacs instead. Also, our patient had no immunizations for the past 20 years, so that is also a concern.
Jessica Bard:
What are your thoughts, Dr. Harrison? Why the headaches? Why the tinnitus? What do you intend to do for him and what do you intend to do with him?
Dr Anil Harrison:
Sure. From your presentation, there have been no symptoms to suggest raised intracranial tension with this patient's headaches, such as nausea or projectile vomiting. His neurological exam has been deemed normal. Although he has bilateral tinnitus, there are no signs to suggest meningeal irritation. There is no focal neurological deficit. So with chronic persistent headaches for six months, besides a thorough neurological exam, I would also like to know what his fundi revealed. I would also like to confirm that there are no carotid bruits or any hums when auscultated over the scalp and the eyeballs.
Jessica Bard:
Right. Those are great thoughts. Another question for you is why does tinnitus?
Dr Anil Harrison:
Okay, so the bilateral tinnitus accompanying his headaches without any vertigo, Jessica, which are constant and without any cyclical episodes. What about his ear exam? I wonder if Rinne's and Weber's tests have been conducted.
Jessica Bard:
Weber's and Rinne's, why?
Dr Anil Harrison:
Well, to evaluate for tinnitus and possible hearing loss and try to ascertain, if there is hearing loss, would it be conduction or sensorineural hearing loss, which would give me an idea to further evaluate possibilities with maybe audiometry and maybe an MRI, MRA of his brain. Those are the things that I would consider and perhaps even an MRV, which is magnetic resonance venography, while trying to rule out structural abnormalities in the brain and the vasculature as well as the venous flow around the brain.
Jessica Bard:
His ear exams were normal. Rinne's and Weber's tests were also non-contributory.
Dr Anil Harrison:
Okay, great. As we know, several pathologies can cause both symptomatic headache and tinnitus, such as carotid artery dissections, arteriovenous malformations, traumatic brain injury, space-occupying intracranial lesions, demyelinating disorders, such as multiple sclerosis. By the way, intracranial, hypo, and hypertension can also give you symptomatic headaches with tinnitus, and of course, on occasion, migraine headaches can also do that.
Jessica Bard:
What is erythromelalgia?
Dr Anil Harrison:
Erythromelalgia is a condition, Jessica, characterized by episodes of pain, redness, and swelling in various parts of the body, particularly the hands and feet. These episodes are usually triggered by an increased body temperature, which may be caused by exercise or entering a warm room. Ingesting alcohol or spicy foods may also trigger an episode. A rule for vascular changes in the pathogenesis of erythromelalgia is suggested by the finding of increased blood flow and they say up to about 10-fold increase as measured by laser Doppler.
On the other hand, there is a suggestion of large and small fiber neuropathy that might be a contributing factor for erythromelalgia. Why the erythromelalgia? Although originally this was described in association with myeloproliferative disorders, such as essential thrombocytosis, CML, polycythemia vera, myelofibrosis, erythromelalgia appears to be associated with underlying myeloproliferative disorders in less than 10% of cases. A diagnosis of myeloproliferative disease may proceed, follow, or coincide with the development of erythromelalgia. Coming to our patient, Jessica, who has diabetes and hypertension and smokes, I would also like to consider neuropathy as well as peripheral artery disease as possibilities for the etiology of his erythromelalgia.
Therefore, putting all three together, the chronic persistent headaches with bilateral tinnitus and erythromelalgia. I wonder if the patient's erythrocytosis is the reason for his symptoms. While we are evaluating this patient, to complete the picture, we also have to evaluate historically for how long has he had diabetes, COPD, and hypertension and how well controlled have they been, what evaluations have been done in the past, and very importantly, if this patient could have a family history of something like a myeloproliferative disorder, early onset COPD, diabetes, hypertension, and vascular events.
Jessica Bard:
Great thoughts. While you're going through your thought process, what in particular have you been looking for in this patient's physical examination if you have to reevaluate?
Dr Anil Harrison:
Sure, Jessica. Following this, even though I have a complete physical exam which has been mentioned as normal except for mild bilateral pitting pedal edema, these are the things that I'm going to think of. I want to see this person's fundi to look for pedal edema. I also want to do a visual field examination as well. I want to examine his mouth, to assess for a Mallampati score and perhaps even a Ferguson tongue score. I would like to measure his neck circumference as a consideration for obstructive sleep apnea. While auscultating, I would like to focus on does he has a parasternal heave.
Does he have a loud P2? Those are things to assess for pulmonary hypertension. I would also like to feel for his liver and spleen. Could he have polycythemia vera or could he have cirrhosis of the liver with long-standing alcohol intake? I would like to assess him for clubbing and cyanosis, markers for hypoxia, or intra and extra-cardiac shunts. I definitely want to feel his peripheral pulses to evaluate for peripheral artery disease given his several comorbidities and the fact that he also has erythromelalgia. Now the pedal edema that you mentioned, the question is, is that iatrogenic, because he's on amlodipine, or could it be secondary to left or right heart failure or could it be because of cirrhosis of the liver or does this patient have varicose veins?
While thinking about etiologies with either increased hydrostatic pressures or reduced oncotic pressures in the veins, I would like to conduct those examinations. Now, I would also like to look for peripheral signs of chronic liver disease. With his history of significant alcohol consumption, and his social life, could he also have hepatitis C resulting in cirrhosis? Of course, I'd like to evaluate him for neuropathy, because of his diabetes and his alcohol consumption, and as a possibility, could he have polycythemia vera? Therefore, summarizing and considering our patient is a large male with a BMI of 35, there are several things to be considered, his neck circumference, and his Mallampati score.
Could his erythrocytosis be secondary to sleep apnea and hypoxia along with hypercarbia? I would look for a parasternal heave, auscultate for a loud P2, and check to see if he has any evidence of right heart failure. With his history of smoking, I would be looking for cyanosis and clubbing as well as feeling his distal pulses at the posterior tibial and the dorsalis pedis to see if he has any evidence of PAD. Because of his diabetes, I would be looking for signs of neuropathy, and because of his erythrocytosis, his lifestyle, and possible excessive alcohol intake, I would also be looking for peripheral signs of chronic liver disease, such as cirrhosis, while examining his belly for hepatosplenomegaly and possible ascites.
Jessica Bard:
Sure, thank you. What are your thoughts on this patient's lab results?
Dr Anil Harrison:
My thoughts, Jessica, with his H/H of 16.7 and 49, he has a normal white cell count and a normal platelet count. I would like to get a CDC with a differential to evaluate for a bit more information, especially on the differential on the WBCs. Are there any immature cells? Does this patient have basophilia? Because of his elevated H/H, I would like to do an iron panel to rule out iron excess, such as hemochromatosis. I would certainly want to do an LFT, because of his erythrocytosis and his increased alcohol intake. I would like to perhaps get a sed rate and a CRP.
These are markers, which would help ascertain the severity of an underlying disease or disorder that the patient might have. Now with an H/H that is elevated, I certainly would want to get serum erythropoietin levels. This would help in the evaluation of erythrocytosis to see what the bone marrow response is. Is his erythropoietin driving the erythrocytosis or is his erythrocytosis secondary to something else? I would also like to get a pulse ox with his erythrocytosis, with his history of tobacco use. The other thing is we have only one value on his testosterone. As we know testosterone levels are highest in the morning and lowest in the afternoon, with physical activity, food stress, and the amount of body fat, which can influence the levels, and therefore, I would like to get a repeat testosterone level at about 8:00 in the morning.
Depending on if the second level comes back low or normal, further testing might be required by getting perhaps an FSH, a follicular stimulating hormone, a luteinizing hormone, and prolactin levels. The other thing is his potassium is low. Now people might say, "Well, he's on chlorthalidone, or it could be something else, which is causing the hypokalemia." I doubt the low potassium would be because of reduced consumption of potassium, which is a rare cause of hypokalemia. The question is whether the patient is losing potassium in the stools though there is no history of diarrhea, could the patient be losing potassium in the urine, especially if we actually hold chlorthalidone for a few days and then repeat a serum potassium and also do a urine potassium to creatinine ratio.
If the ratio is less than 13 in the urine, it would point to extra-renal causes, such as poor ingestion loss in the stools or transcellular shifts, as opposed to if the potassium creatinine ratio is greater than 13, then this would point towards renal losses of potassium, such as what occurs with the stimulation of the renin-angiotensin-aldosterone system. The other point is why was a PSA done. My question on a PSA would be it might've been a shared decision between the patient and the physician realizing the issues with doing a PSA unless the patient has a significant family history of prostate cancer or has African-American ethnicity. The question is what do we do now?
The other thing I mentioned was a stool guaiac was done, so if it was for colon cancer screening, we need three consecutive samples. Another thing I would do is I would do a urine albumin creatinine ratio because the patient is a diabetic and this would help us gauge if the patient has moderate or severe albuminuria. If negative for urine albumin, that would be a relief. Another consideration would be whether should we conduct spirometry on this patient. The patient has a diagnosis of COPD and I understand his history of smoking. I perhaps would like to get a PFT done and stage his COPD with the gold criteria and with the symptoms to see if the inhalers are enough for this patient. Now, another thing would be should we get an EKG or an echo?
I would say yes, the patient has hypertension, and that too resistant hypertension, because he already is on three antihypertensive, so an EKG is warranted. If on the EKG I find abnormalities, such as left ventricular hypertrophy or any evidence of prior MI, it would give me good enough ground to get an echocardiogram as well. However, this patient has a possibility of sleep apnea. He has COPD, so I think I would go with an echo to see what the pulmonary pressures are and if there is any right ventricular hypertrophy in our patient. I would also like to get hep B, hep C, and HIV.
The WHO recommendations, every patient needs to be checked for hepatitis C and this patient is a diabetic, so I'd like to check him for hepatitis B and with his social life I'd like to at least get an HIV, which is also a recommendation that one needs to get that done on every patient at some point.
Jessica Bard:
What about his elevated triglycerides?
Dr Anil Harrison:
Yeah, Jessica, his triglycerides are 400 milligrams percent and this could be related to his elevated blood sugar, of course, his alcohol, his weight, and his diet. I feel hopefully with lifestyle changes and with better control of his blood sugars, his triglycerides will get better. At this point, with his elevated atherosclerotic cardiovascular disease risk of greater than 20%, putting him on a high-dose statin would be my top priority. With repeat blood work, if his triglycerides are still elevated or are higher, at that point, I might consider starting him on something like icosapent ethyl.
Jessica Bard:
Great. Are there any questionnaires or risk assessment tools that you would utilize, Dr. Harrison?
Dr Anil Harrison:
Absolutely, Jessica. I would do an ASCVD risk score, which has already been done on this patient, it's more than 20%. Because he's a diabetic, we know that he needs to be on at least a moderate dose of statin, but in addition, he has hypertension, he's a smoker, he's in the geriatric age group, and with his ASCVD score of more than 20%, he needs to be on a high dose statin. I would like to calculate his GFR using the Cockcroft-Gault equation, which is 140 minus age, multiplied by body weight in kilograms, divided by 72 times his serum creatinine. I would also like to conduct a STOP-BANG questionnaire, where S stands for snoring, T for tiredness, O for observed apnea, B for blood pressure, B is a body mass index, N is your neck circumference, and G is gender.
A score of three to four is intermediate risk, whereas a score that is five to eight is considered to be high risk for patients having sleep apnea. Besides, I would also like to consider a PHQ-2 and even a PHQ-9, since depression affects an estimated one in 15 adults in any given year, and one in six people, which is about 16%, will experience depression at some time in their lives. Fortunately, there is a better awareness of mental health, Jessica, and I feel at least a PHQ-2 should be ordered on every patient who walks into the clinic, and if positive, this ought to be followed by a PHQ-9. Depression is defined by a score of greater than 10 out of a possibility of a score of 27.
I would conduct an alcohol use disorder questionnaire as well, either a CAGE or a MAST. A standard drink is five ounces of wine, or 12 ounces of beer, or 1.5 ounces of 80-proof spirit. What I do is I ask the patient, how many times has he or she ever had more than five drinks in the past year? If say yes, then I go on to either an AUDIT-C a CAGE, or a MAST questionnaire. With his smoking, I would like to calculate his pack per year smoking history. If you smoke 20 cigarettes a day for a year, that is one pack a year and you multiply it by the number of years that the patient has smoked.
The reason for this is that if a patient has a 20-pack-year smoking history and is either a current smoker or former smoker having quit within the past 15 years, the guidelines are that one needs to get a low-dose helical CT scan of the lungs. The other thing is, that I would also like to see if a patient has heart failure or is at risk for heart failure. Our patient, Jessica, has a sedentary lifestyle, so we really cannot assess his NYHA heart failure stage, although there has been no mention of orthopnea or PND and the patient does not have any significant shortness of breath.
There was no JVD mentioned, there was no positive HJR, there was no LVS-3 or LVS-4 and the cardiac apex was not displaced. Therefore, he probably does not have NYHA class four heart failure. Though given the fact that he has diabetes, hypertension, probably sleep apnea, he's elderly, he's male, he is at risk for heart failure.
Jessica Bard:
You mentioned his sedentary lifestyle. Out of curiosity, as a YouTuber, how many mets does he burn? What is metabolic equivalent and what are some other considerations you might have for this patient when you're evaluating him?
Dr Anil Harrison:
Sure, Jessica. A met or metabolic equivalent is widely used in the cardiovascular population exercise guidelines. It's actually a means of quantifying the energy demands of physical activity. It relates the rate of the body's oxygen uptake, called the VO2, for a given activity as a multiple of an individual's resting VO2. You'd agree, Jessica, with his very sedentary lifestyle, he probably burns no more than one met. This would be different if he were jumping rope, that would be approximately 10 METS.
Jessica Bard:
Would you say that he has CKD?
Dr Anil Harrison:
Chronic kidney disease is defined as the presence of kidney damage, usually detected as a urinary albumin creatinine ratio greater than 30 milligrams per day or equivalent, or decreased kidney function where the GFR is less than 60 ml per minute. This has to be over three months irrespective of the cause. Therefore, to answer your question, I would wait to calculate this patient's GFR and his urine albumin creatinine ratio before we say whether he might have CKD or not.
Jessica Bard:
Is he at risk for falls? Talk to us about his fall risk assessment.
Dr Anil Harrison:
Sure, Jessica. An assessment of fall risks should be integrated into the history and physical exam of all geriatric patients, including those not specifically being seen for a problem with falling. All older patients or caregivers should be asked at least once a year about falls, and the frequency of falling. Are there any difficulties in gait or balance? For patients who report a single fall, gait and balance deficits should be evaluated as a screen for identifying individuals who may benefit from a multifactorial fall risk assessment.
A multifactorial fall risk assessment should be performed for community-dwelling older persons who report recurrent, which means two or more falls, who report difficulties with gait or balance, and who seek medical attention or present to the ER because of a fall. When this patient is in the office. Besides asking the above questions, one could conduct a getup-and-go test. The test is performed by observing the subject rising from a standard armchair, walking a fixed distance across the room, turning around walking back to the chair, and sitting back down.
While doing this, observation of the different components of this test may help to identify deficits in leg strength, balance, vestibular function, and gait. The timed part of the test records the mean time, in seconds, from initially getting up to re-seeding and patients are then compared with the mean time of adults in their age group of be it 60 to 69, 70 to 79, and 82 to 99.
Jessica Bard:
Does he have PAD?
Dr Anil Harrison:
That's a great question. Since the patient has several risk factors for peripheral artery disease and with his lifestyle, the question is whether PAD precludes him from walking. Therefore, more questions need to be asked if he has any symptoms to suggest claudication, and while examining, looking for dermatological and vascular changes, especially in the lower extremities, listening for bruit and feeling for distal pulses are very important.
Jessica Bard:
Could he have CAD?
Dr Anil Harrison:
Could he have coronary artery disease? Another great question. Since the patient has several risk factors, a sedentary lifestyle, diabetes, hypertension, hyperlipidemia, and tobacco, the probability is high that he has coronary artery disease. I would start by doing an ASCVD risk assessment, which includes race, sex, age, total cholesterol, HDL cholesterol, and systolic blood pressure. If the patient is on medication for hypertension, the patient is a diabetic and the patient smokes. Our patient has an ASCVD risk of greater than 20% and he would benefit from a high dose statin along with the baby aspirin to be taken every day.
Jessica Bard:
What are the chances of him having fatty steatosis cirrhosis?
Dr Anil Harrison:
I think without an ultrasound or LFTs it is difficult to say, but with his body habitus his drinking issues, and his weight, there is a good chance that he might have at least fatty steatosis, if not cirrhosis.
Jessica Bard:
Would you recommend an ultrasound of his abdominal aorta and what are some of the screening tests that he would conduct?
Dr Anil Harrison:
Jessica. We recommend a one-time screening for abdominal aortic aneurysm with an abdominal ultrasound in men aged 65 to 75 who have ever smoked. Screening for an aneurysm in men over age 65 is associated with a decreased risk of abdominal aortic aneurysm mortality.
Jessica Bard:
What does one do with a mildly elevated PSA such as his, repeat a PSA, a DRE, or a biopsy?
Dr Anil Harrison:
The serum PSA is a valuable marker, Jessica, for prostate cancer, however, its sensitivity and specificity are not perfect as a screening tool. An elevated PSA value can also be due to many other causes. One promising method to improve the specificity of PSA testing for men who have total values of four to 10, just as our patient does, and to improve sensitivity at levels below four is to include PSA isoforms such as free to total PSA ratio.
The percentage of free PSA to total PSA has been used to improve the sensitivity of cancer detection when the total PSA is in the normal range, and to increase the specificity of cancer detection when it is in the gray zone of four to 10. In the latter group, the lower the value of free to total PSA, the greater the likelihood that an elevated PSA represents cancer and not BPH. Another approach has been to assess the rate of PSA change over time, which is called the PSA velocity. An elevated serum PSA that continues to rise over time is more likely to reflect prostate cancer than one that is consistently stable. In one study, a PSA velocity cutoff at 0.75 nanograms per ml per year distinguished patients with prostate cancer from those with either BPH or no prostate disease with a specificity of 90 to 100% respectively.
Therefore, what I would do, since the patient does not have a family history of prostate cancer, the possibility is could the slight elevation of PSA be due to BPH or could be prostate cancer. Therefore, I would repeat a PSA along with a free PSA in about six months to a year. If the free PSA to total ratio is low, or if the PSA velocity in a year has gone up to 0.75, the chances are that this is prostate cancer. If not, then it's BPH.
Jessica Bard:
Would you do other tests, such as BNP, D-dimer, urinalysis, EKG, echo, sputum for malignant cytology, urine for malignant cytology, ultrasound of his liver, or anything like that?
Dr Anil Harrison:
Yeah, those are great questions, Jessica. Our patient could have elevated BNP because of left heart failure, right heart failure, and COPD, and he also has a high probability of sleep apnea. With his renal function not being the best, we feel that the BNP would be elevated. The recommendations are that if the patient is admitted with a diagnosis of heart failure, getting a BNP and a serum troponin would help, prognostically, although following levels of BNP would not be a good idea. You mentioned that our patient has a mild elevation of BNP.
The other question you asked me was, would I do a D-dimer? Again, a dimer can be elevated because of several reasons and I would do it only if I'm considering a possibility that suggests something like a DVT or a pulmonary embolism. With his good score of zero, DVT seems unlikely. If it were greater than two, then I would consider DVT as a probable etiology. As we know, if it's between three to eight, then the probability is high. That is a time I'd be concerned about, but with a good score of zero, I probably would not get a D-dimer.
Jessica Bard:
His D-dimer was negative.
Dr Anil Harrison:
Therefore, I would look no further.
Jessica Bard:
Would you do a urinalysis?
Dr Anil Harrison:
I would not do a urinalysis without any symptoms and without any red herrings, though, as I mentioned, I would get a urine vial albumin creatinine ratio.
Jessica Bard:
His urinalysis was negative. Would you check sputum for malignant cytology?
Dr Anil Harrison:
I would not. He has no symptoms of lung cancer, and in addition, sputum for malignant cells has limitations for molecular and histochemical staging. Getting a piece of the tissue if he has cancer is better, and staging it with imaging studies would be the way to go. Only if the patient refuses a biopsy, we consider sputum for malignant cytology, which has a 42 to 97% sensitivity for non-small cell lung cancers.
Jessica Bard:
Would you do urine for malignant cytology?
Dr Anil Harrison:
Urine cytology has a relatively poor sensitivity, particularly for low-grade tumors. Most urine-based molecular markers are more sensitive than urine cytology in the detection of urothelial cancers, specifically for low-grade tumors, but the specificity of molecular markers is inferior to that of urine cytology.
Jessica Bard:
Would you do an ultrasound of his liver?
Dr Anil Harrison:
I think that's reasonable, especially if we find some abnormalities on his LFT, and if one finds a fatty liver, then getting a FibroScan subsequently would be the best thing to do.
Jessica Bard:
What is your approach to erythrocytosis?
Dr Anil Harrison:
Erythrocytosis, and Jessica, is if the hemoglobin is greater than 16 in women and greater than 16.5 in men. While thinking about erythrocytosis, the consideration should be this relative erythrocytosis, that is without an absolute increase in the RBC mass. This could happen because of a loss of plasma volume. If the above is not the case, then you have to consider is it primary polycythemia caused by a mutation such as polycythemia vera or is it secondary polycythemia, because of hypoxia, or could it be because of an erythropoietin-producing tumor, such as hepatocellular carcinomas, renal cell carcinomas, hemangioblastomas, pheochromocytoma, and uterine myomas.
The first thing I would do is exclude dehydration, which would account for relative erythrocytosis. Remember, our patient was on chlorthalidone or is on chlorthalidone. The second thing I would do is I would check erythropoietin levels. I think this patient is on an SGLT2 inhibitor and SGLT2 inhibitors can cause elevated erythropoietin levels we've mentioned other reasons for elevated erythropoietin, being hypoxia and the tumors that, erythropoietin-producing tumors. Of course, remember a patient probably has hypoxia. He is a smoker, he's living at a very high altitude. He might have secondary polycythemia. If the erythropoietin levels are normal, it is only then that I would do a JAK2 V617F, and perhaps, a JAK2 exon 12 mutation.
If that is positive, this points towards polycythemia vera. In our patient, his CBC with differential showed no leukocytosis. There was no thrombocytosis. This patient had no basophilia. He reported no post-bath pruritus. He had no splenomegaly and his serum erythropoietin levels were elevated, so his erythrocytosis has secondary causes and I would not do any genetic markers looking for polycythemia vera. Etiologies for our patient's erythrocytosis, I feel, are related to hypoxia and elevated carbon monoxide from smoking. It could be because of high altitude, it could be because of sleep apnea, and of course, as I mentioned, it could be because he's on an SGLT2 inhibitor.
Jessica Bard:
Should we worry about his low potassium?
Dr Anil Harrison:
Yeah, Jessica, so the concerns are low potassium and hypertension and the patient is on three blood pressure medications. This is called resistant hypertension. Though I understand he's on chlorthalidone, the hyperkalemia is concerning. If you also think about he's on lisinopril and his kidneys are not the best, so you might have expected hyperkalemia instead, but if you're still not sure, you could take the patient off chlorthalidone for a few days and repeat another serum potassium.
If it's still low, I would do a urine-potassium creatinine ratio. If elevated, it suggests renal losses, which could be secondary to a hyperaldosteronism state. While discussing his resistant hypertension, I would also like to mention that his probable sleep apnea could also be a contributing factor to his resistant hypertension.
Jessica Bard:
How would you go about evaluating for hyperaldosteronism, given the fact that the patient has resistant hypertension and hypokalemia?
Dr Anil Harrison:
Yeah, Jessica. I would consider a serum aldosterone and renin level and do a ratio of aldosterone to renin. If the ratio is less than 20 years to one, that is secondary hyperaldosteronism. Things like renal artery stenosis, cirrhosis, cardosis, or heart failure would be considerations. If the ratio of aldosterone to renin is greater than 20 years to one, then one has to consider the possibility of primary hyperaldosteronism, following which, you could do a salt loading test, and if positive a CT or an MRI of the adrenal glands evaluating for primary hyperaldosteronism. Remember, in 25% of the cases, it is because of an adrenal adenoma, whereas in 75% of the cases it is actually because of adrenal hyperplasia.
Jessica Bard:
What do you think could be the reason for this patient's secondary hyperaldosteronism? And by the way, this patient's diuretic has been held for several days before conducting this test.
Dr Anil Harrison:
Jessica, therefore the diuretic use probably has been ruled out as an etiology for his secondary hyperaldosteronism. His secondary hyperaldosteronism could be either because of renal artery stenosis or because of cirrhosis of his liver. I don't think he has nephrotic syndrome, and since there is no history of vomiting diarrhea, or low intake of salt, I would like to consider possibility of renal artery stenosis in this patient.
Even though on clinical exam there were no renal bruits, that should not preclude one from evaluating for renal artery stenosis given the fact that the patient's creatinine was also elevated, I would therefore start with a non-invasive mode of getting a duplex renal artery ultrasound, and if required, follow it up with either an MRA or a CTA. Having said that, if one discovers renal artery stenosis most often surgical intervention is not required. Instead, one intensifies medical therapy, which would be more appropriate.
Jessica Bard:
What are your thoughts on the evaluation of the renin-angiotensin aldosterone system? We calculated the patient's GFR at 70.
Dr Anil Harrison:
By the way, I was going to this patient's records and I found that he had a duplex renal artery ultrasound, and subsequently, a magnetic resonance angiography of his renal arteries and it revealed bilateral renal stenosis, and renal artery stenosis. The stenosis was less than 60% with less than 180 centimeters per second flow velocity across the stenosis. There is mild echogenicity, but normal-sized kidneys.
Jessica Bard:
Which intervention would be best? Would you also consider holding his ACE inhibitor with an elevated creatinine and low GFR?
Dr Anil Harrison:
I would not hold off on his ACE inhibitor, Jessica, and will only consider doing that if the GFR goes below 30% or the serum potassium goes above 5.6 M equivalents per liter. Some folks would actually cut back on the dose of an ACE inhibitor in this scenario reevaluate creatinine and potassium and then make a decision. If you see, our patient's potassium is low and as GFR was 70, I would continue his ACE inhibitor due to the benefits of these medications reducing intraglomerular pressure and preventing subsequent kidney damage.
The other thing is, Jessica, you had questions on which intervention would be considered as of now, given the fact that the patient has bilateral renal artery stenosis. I agree that the patient has bilateral renal artery stenosis. Still, it does not seem to be significant with the measurements that you have mentioned of the stenotic lesions and the velocity across the stenosis. Therefore, I recommend medical management with ACE inhibitors or angiotensin receptor blockers while following the patient's creatinine and potassium. If the GFR and the potassium are stable, then we are doing fine using these medications.
Very importantly, I would also consider better management of his diabetes, putting this patient on an aspirin along with a statin. Somebody had asked me about the indications of putting a stent or doing an angioplasty for renal artery stenosis. The indications for unilateral renal artery stenosis for stent placement or angioplasty are a short duration of blood pressure elevation before the diagnosis of renal vascular disease since this is the strongest clinical predictor of a fall in blood pressure after renal revascularization, or if there's a failure of optimal medical therapy to control the patient's blood pressure, or the patient is intolerant to optimal medical therapy, or if the patient encounters flash pulmonary edema and/or refractory heart failure.
Those are my thoughts, Jessica. Once again, our patient's ASCVD risk score is more than 20% his urine albumin creatinine ratio is 60, his fundi show background diabetic retinopathy, his pulse ox is low at 85% on room air, and evaluating sleep apnea in a patient has a MALLAMPATI score of three out of four and a stop bank score of more than five.
Jessica Bard:
With all this information, what would you say he's at risk for and could you share your thoughts on that?
Dr Anil Harrison:
Yeah, absolutely. This patient is at very high risk for coronary artery disease. An ASCVD risk assessment must be done for everyone between ages of 40 to 75. Folks not only have a higher risk for coronary artery disease but also heart failure, TIAs, strokes, peripheral artery disease, and thoracic and abdominal aortic aneurysms. Therefore, besides better diabetes and hypertension control, he needs to be on a high-dose statin along with aspirin.
The other thing, Jessica, is that his fundoscopic exam revealed non-proliferative diabetic retinopathy and his albumin creatinine ratio of 60 confirms moderate microalbuminuria. These represent the patient's microvasculature have already been affected and confirm significant primary prevention opportunities with lifestyle modifications, such as tobacco cessation, better diabetes control, better blood pressure control, and putting the person on a high dose statin and aspirin. The other thing is his pulse ox of 85% on room air confirms that the patient has hypoxia, either because of COPD or perhaps the high altitude and this patient needs to be on oxygen at all times to keep his saturation above 90%.
Another thing is, with our patient who has a Mallampati score of three, which means when only the soft palate and the base of the uvula are visible and with a STOP-BANK score of greater than five, he has a very high probability of obstructive sleep apnea. I was reading through the notes and I found that this patient had an apnea-hypopnea index score of greater than 30, which means that he has severe sleep apnea.
Jessica Bard:
What would you recommend? Oral appliance, orthodontic surgery, CPAP, BiPAP?
Dr Anil Harrison:
Yeah, so an AHI, or apnea-hypopnea index, the RDI stands for respiratory disturbance index and the REI represents respiratory event index. If the values are between five and 14, this constitutes mild sleep apnea, 15 to 30 as moderate, and anything over 30 as severe sleep apnea. How important is this? Well, the number might just be numbers. The fact that the patient has severe sleep apnea puts them at several risks, such as neuro-psych issues with irritability and inattentiveness. Also, the patient is at high risk for motor vehicle accidents.
Besides, he's at very high risk for coronary artery disease, heart failure, arrhythmia, stroke, pulmonary hypertension, type two diabetes, gout, fatty liver, et cetera. Of these, the patient already has type two diabetes and hypertension, and as we evaluate him, other possibilities might come up. Another thing is, that obstructive sleep apnea, should be approached as a chronic disease that requires long-term multidisciplinary management. The potential benefits of successfully treating sleep apnea include clinical improvements, for example, less daytime sleepiness, reduced healthcare utilization and costs, and possibly decreased cardiovascular mortality and morbidity.
Therefore, besides lifestyle changes, such as weight loss, and avoiding alcohol and tobacco, behavioral therapies also need to be instituted. Our patient with severe sleep apnea, needs positive airway pressure with either CPAP or BiPAP. If he had mild to moderate sleep apnea and the patient refused a CPAP or a BiPAP, in those instances, oral appliances could have been considered. The goals of sleep apnea therapy are to resolve signs and symptoms of sleep apnea, improve sleep quality, and normalize the apnea-hypopnea index along with the oxyhemoglobin saturation levels.
Jessica Bard:
What about surgery, such as bariatric surgery?
Dr Anil Harrison:
Great question, Jessica. The recommendations are that one has to try positive airway pressure therapy first and give it about three months before considering oral surgery or bariatric surgery. Once again, a patient with diabetes with a hemoglobin A1C of 7.8 is kind of okay for a 65-year-old person.
Jessica Bard:
Does he need a dietician or a diabetic educator? Does his creatinine or GFR preclude him from using metformin?
Dr Anil Harrison:
Yeah, so most adult patients should have a hemoglobin A1C below seven, which gives an indirect measurement of the fasting blood sugars being below 130-milligram percent and the two-hour postprandial blood sugars being below 180-milligram percent. In the elderly, having a hemoglobin A1C greater than eight is perfectly reasonable. Given his significant comorbidities, I would recommend having the patient see a dietician and a diabetic educator. To answer your question, Jessica, his GFR of 70 does not preclude him from being on metformin.
Only if the GFR were less than 45, I would consider halving or reducing the dose of his metformin, and if his GFR went below 30, that would be the time I would take him off metformin, otherwise not. The reason for that would be that lower GFRs predispose a person to lactic acidosis, especially with compromised renal functions. I think one of the residents had asked me this question, would you consider holding off on the SGLT2 inhibitors, because we said the secondary erythrocytosis that the patient had could be because of that?
Now that is a great question, considering that this patient's erythrocytosis might be secondary to the SGLT2 inhibitor, although we have several other reasons for this patient to have secondary erythrocytosis, we know that SGLT2 inhibitors are cardioprotective and are renal protective, and therefore, I would tend to continue the SGLT2 inhibitors and monitor the patient's H/H. If the H/H did not improve or was getting worse, then I would probably consider taking the patient off the SGLT2 inhibitor and replacing it with, let's say, a GLP-1 agonist, which is also cardioprotective. The GLP-1 agonist along with metformin would be argued for better diabetes control, weight loss, and cardiovascular benefits.
Another question posed by a resident was how often do you intend to check the hemoglobin A1C, the urine albumin creatinine ratio, doing a retinal exam, doing a foot exam? The answer to that is that hemoglobin A1C can probably be checked maybe twice a year, especially if the diabetes is under reasonable control. If it weren't, then I would recommend checking it every three months. For retinal eye exams, once a year is what is recommended.
Jessica Bard:
Which antihypertensive would you consider and why?
Dr Anil Harrison:
I would probably consider putting him on spironolactone with the added advantage of addressing his low potassium and the possibility of a mineralocorticoid excess as discussed before. As a word of caution with spironolactone, serum potassium, and renal functions should be checked three days after you start the medication, then in a week, and then at least monthly for about three months, followed by quarterly for about a year. If adding or increasing the dose of concomitant ACE inhibitors, or ARBs, a new cycle of monitoring should be done. Remember, if serum potassium goes above 5.5 or renal functions worsen, the advice would be to hold the spironolactone until the potassium gets to below five ml equivalents per liter, and then, you can certainly consider restarting with a reduced dose after confirming the resolution of the hyperkalemia and the renal insufficiency for at least 72 hours.
Jessica Bard:
Any reasons for our patient having plus one pitting pedal edema?
Dr Anil Harrison:
Yeah, so in our patient with resistant hypertension and one plus pitting pedal edema, my thoughts are it could be because of the amlodipine the patient is on, or it could be because of core pulmonology secondary to his COPD or sleep apnea. It could be because of his hypertension, it could be because of heart failure, it could be because of dependent edema with varicosities, and of course, he might have a fatty liver and/or cirrhosis that could also cause lower extremity pitting pedal edema. The other thing you mentioned, the EKG on this patient showed right ventricular hypertrophy and P pulmonale. My thoughts would be that this probably is secondary to COPD with cor pulmonale or it could be because of sleep apnea with right ventricle failure. Of course, one has to think about chronic pulmonary thromboembolism as an etiology, since our patient is pretty much sedentary.
Jessica Bard:
The echo reveals normal left chambers, EF55, left ventricular diastolic dysfunction, and pulmonary pressures of more than 30. What are your thoughts there?
Dr Anil Harrison:
Yeah, so this tells one that this person has a diastolic dysfunction along with moderate to severe pulmonary hypertension. Fortunately, his ejection fraction is 55, which is okay, slightly below normal or at the cusp I would say. Those are my thoughts on this patient. It does happen on spironolactone that once in a while a patient can develop painful gynecomastia, and in that scenario, switching the spironolactone to eplerenone would be a reasonable idea. This patient has one or two plus pitting pedal edema. Stemmer sign is something that is done to see if a patient might have lymphoedema, where you pinch the skin over the dorsum of the foot, and if you can't, then it possibly points towards either lymphedema or the person might be significantly obese.
With fluid edema, you can lift the skin, so that would be a negative Stemmer sign. Our patient has several reasons, as mentioned, for pedal edema, sleep apnea, and COPD with cor pulmonale. Of course, his diastolic dysfunction puts him at heart failure with preserved ejection fraction, it could be hydrogen because of the calcium channel blocker that the patient is on. Another question from the resident is what are your thoughts on our patient with chronic headaches and bilateral tinnitus, since the MRI, MRA, and MRV of the brain were normal? As discussed before, other etiologies for chronic headaches and bilateral tinnitus with a good neurological exam and imaging studies have ruled out several etiologies, and therefore, I feel his chronic headaches and bilateral tinnitus might be related to his erythrocytosis.
Fortunately, the patient is on aspirin now and we hope that his erythrocytosis should respond to discontinuing tobacco, holding off on chlorthalidone, with better treatment or with better control of his COPD, and if this patient is on a CPAP, hopefully, the hypoxia and the hypercarbia should improve and that should probably take care of his erythrocytosis. The other thing is he's at a high altitude, whether he can move to sea level, that should also help his erythrocytosis. If all these measures do not help, and of course we rule this patient out for polycythemia vera, then one might consider phlebotomies, drawing out blood to reduce the red cell mass, and reduce the hemoglobin and hematocrit in this patient.
Jessica Bard:
In attempting to help our patient, what else do you recommend?
Dr Anil Harrison:
Jessica, I would recommend lifestyle modifications, a heart-healthy diabetic weight, and reducing diet with exercise. I'd probably offer tobacco for his tobacco cessation, varenicline or Chantix along with nicotine replacement therapy and behavioral therapy, which is superior to bupropion or Wellbutrin plus nicotine replacement therapy and behavioral therapy. I would also have him stop his alcohol. One could consider cognitive behavioral therapy along with naltrexone, which is better than acamprosate and cognitive behavioral therapy. Of course, descending from Mount Taos, where he lives at an altitude of approximately 11,000 feet, should certainly help his secondary erythrocytosis.
Jessica Bard:
What would your considerations be as far as immunizations and cancer screenings go?
Dr Anil Harrison:
Yeah, that is a great question, Jessica. Consider FIT testing. His average risk, doing a FIT, or a fecal immunochemical testing, would be absolutely fine unless a patient agrees to a colonoscopy. There are other modalities as well, stool guaiac times three or a Cologuard. Because he's a smoker and he's in the age group, I would also recommend a low-dose CT chest as far as cancer screening goes. Now, he's completed his vaccinations or his immunizations until about 20 years ago. At this point, I would recommend him getting a PSV20 pneumococcal vaccine.
I would also recommend a Tdap, a Shingrix vaccine. I would, of course, recommend the COVID vaccine, and come October recommends the influenza vaccine, and of course, the hepatitis B vaccine as well. Another consideration would be if he says, "Well, what about surgery?" The other thing to consider is surgery for sleep apnea and/or bariatric surgery. Although the guidelines are that the patient should have tried positive airway pressure ventilation for at least three months, only then you could consider either bariatric surgery or oral surgery.
Jessica Bard:
How would you plan follow-up care and visits for our patient?
Dr Anil Harrison:
Yes, absolutely. The patient's hemoglobin A1C for his age, I think, is okay, but I could consider putting him on metformin because metformin like the SGLT2 inhibitor or the GLP-1 agonist does not cause hypoglycemia. I would continue with the SGLT2 inhibitor with considerations of using semaglutide orally or once weekly injection as a GLP-1 agonist. Make sure that before you start a GLP-1 agonist, you rule out a family history of medullary carcinoma of the thyroid and the MEN1 syndromes, along you want to make sure that the patient doesn't have a history of pancreatitis.
Then I would check hemoglobin A1C in about three to six months, and perhaps maybe once or twice a year thereafter. I would certainly put him on aspirin, 81 milligrams a day. I would put him on high-dose atorvastatin or rosuvastatin. I would continue his ACE inhibitor amlodipine and add spironolactone. I would put him on oxygen by nasal cannula to keep his saturation above 90% and check his oxygen saturation in about two or three days. I would make sure that he is using his CPAP machine. The thing that I forgot to mention with a statin is before I start him on a statin, I would like to get an AST, an ALT, CPK, and a TSH, and if they're normal, then I would put him on a high dose statin and check his lipids in about six weeks with goals of trying to get his LDL cholesterol to be definitely below 100-milligram percent, preferably below 70-milligram percent.
On spironolactone, as I mentioned, I would check his potassium and creatinine in three days, then in a week, and then once monthly for three months, and then every three months subsequently. I would have him monitor his blood sugars to keep most of his fasting blood sugars below 130 and his two-hour postprandial blood sugars below 180 milligrams percent. I would like his blood pressure to be definitely below 130/80 millimeters of mercury. I would have him monitor his weight weekly and I would recommend getting an echocardiogram in three to six months to evaluate his pulmonary pressures because if the pulmonary pressures have improved, this would be a good sign.
Since pulmonary hypertension, secondary to sleep apnea is probably the only etiology for treatable pulmonary hypertension. We see that he had a low testosterone level. I would repeat his 8:00 AM testosterone levels. I would have a nurse call him in two weeks to see how he's doing and probably do a telemedicine visit with him in about six weeks, and I would plan for maybe a three to six-month in-person evaluation.
Jessica Bard:
Right. I've got lots of other questions here. Which statin would you choose? What would you consider doing before starting the patient on a statin? When would you consider checking lipids? When would you consider checking liver enzymes? What if his LDL cholesterol does not come to the desired level? What if his triglycerides do not budge?
Dr Anil Harrison:
Great question. I would check AST and ALT along with a CPK and TSH before starting the patient on a statin, check lipids in six weeks to make sure they are where they ought to be, and then perhaps check them in a year. Checking liver enzymes after you've started a patient on a statin, is probably recommended only if the patient becomes symptomatic, or is jaundiced, only then do you check for liver enzymes. As far as the dose of the patient's statin, he already is on the maximum dose and is compliant with lifestyle changes.
If I had to add something, I'd probably consider ezetimibe, also called Zetia, to get his LDL cholesterol where we want it to be. His triglycerides should come down as his diabetes and his weight are under a bit of control and he has cut back on his alcohol. I would not use gemfibrozil given its track record when combined with a statin. If the triglycerides do not budge, I could probably consider icosapent ethyl in this patient.
Jessica Bard:
Could you give us a few side effects of SGLT2 inhibitors? What are some of the important things to consider before initiating GLP-1 agonists? How often do metformin, GLP-1, and SGLT2 inhibitors cause symptomatic hypoglycemia?
Dr Anil Harrison:
Yes, Jessica. SGLT2 inhibitors, besides causing glycosuria and polyuria, can result in significant fluid losses. They can cause non-ketotic diabetic ketoacidosis and predispose one to urinary tract infections and genital fungal infections. The SGLT2 inhibitors need to be held as the GFR drops below 30. Before starting a person on a GLP-1 agonist, MEN1 or multiple endocrine neoplasia one syndrome and medullary carcinoma of the thyroid, especially a family history along with a history of pancreatitis should be ruled out.
Jessica Bard:
Our patient has low testosterone levels. My questions here are what could be the reasons for that? Do you think he could be symptomatic because of this? What treatment considerations would you have and would you consider any labs? In general, what are your biggest concerns here?
Dr Anil Harrison:
Yes, Jessica. This patient has plenty of reasons for low testosterone, smoking, obesity, diabetes, hypertension, his hyperlipidemia, and of course, sleep apnea. I would not be surprised that this patient has low libido as well as erectile dysfunction. You see the testicles are a vascular bed, which are stimulated by follicular stimulating hormone through these seminiferous tubules to produce sperms. The luteinizing hormones, stimulate the Leydig cells to produce testosterone.
Most of the testosterone is in the bound form, I would say about 98%, and only about one to 2% is free testosterone. As one age, one's sex hormone binding globulin levels increase as they also do with HIV. Conversely, your sex hormone binding globulin decreases with diabetes, because we know that testosterone can elevate blood pressure as well as result in elevated hemoglobin and hematocrit, and with his borderline elevated PSA, I would be skeptical about starting him on testosterone therapy. Besides, we also need another testosterone level before we say that his testosterone levels are low.
Jessica Bard:
Would you consider repeating an echo and why?
Dr Anil Harrison:
I would recommend getting an echo in about three to six months to see how his pulmonary hypertension is doing. Once we confirm low testosterone, his borderline elevated PSA is thought to be related to BPH and his H/H comes down and his blood pressure also comes down, then one could consider initiating testosterone therapy, otherwise not. But again, before I do that, I want a baseline CBC, I want a baseline PSA to be normal. In the interim, what we could offer the patient are PDE5 inhibitors for erectile dysfunction.
Jessica Bard:
Regarding the low testosterone, what do folks usually present with? What percentage of folks with erectile dysfunction have low testosterone? How and what treatment modalities would you consider? How long would you consider treating and would you consider a testicular ultrasound? Would you consider an MRI of the brain?
Dr Anil Harrison:
Great questions, Jessica. Up to about 60% of people with low testosterone have erectile dysfunction. If we confirm that the patient has two low readings of testosterone, measuring luteinizing hormone, follicular stimulating hormone, and prolactin levels should be included to determine if the problem is primarily in the testicles, which would have low testosterone levels and normal to elevated FSH and LH levels. Conversely, if it is secondary to pituitary causes, one would have normal to low levels of LH and FSH along with low testosterone. Most causes are central.
The three important symptoms of low testosterone are low libido, erectile dysfunction, and poor penetration. Treatment modalities are either parenteral testosterone therapy, which is the best way to administer testosterone, or you could choose oral, nasal, or transcutaneous preparations of testosterone. I would not recommend an ultrasound of the testicles unless one discovers an abnormality and palpation. If secondary central causes are considered as a reason for low testosterone, you could consider getting an MRI of the brain if a person has signs of raised intracranial tension, or has, let's say, papilledema or visual field defects, and if the testosterone on two readings is less than 150, then you might think, could the person have a pituitary tumor?
Jessica Bard:
To close our conversation today, please give us a summary of our patient.
Dr Anil Harrison:
Sure, Jessica, I can try. We have a male in his mid-60s with type two diabetes, hypertension, hyperlipidemia, and a 30-pack-year history of tobacco use and with 20 years of consuming three ounces of 60% proof liquor with an exercise capacity equaling one met, residing at high altitude was discovered to have secondary erythrocytosis as the etiology for his chronic headaches, bilateral tinnitus and erythromelalgia, which resolved a month ago on aspirin and lifestyle modifications along with the medications that we put the patient on and CPAP. Spironolactone was initiated for his resistant hypertension, which seems to be doing better.
He has type two diabetes mellitus with microvascular disease and CKD G2 A2 and he is on metformin, canagliflozin, ACE inhibitor, high dose statin, along with 81 milligrams of aspirin. His ASCVD risk score is greater than 20% and he is at risk for heart failure. He has confirmed renal artery stenosis, and hence, peripheral artery disease and other atherosclerotic diseases with plans to intensify medical management to prevent surgical interventions. My evaluation confirmed COPD Gold three for which he is on maximum doses of LAMA, LABA, inhaled corticosteroid, and rescue inhaler along with three liters of oxygen by nasal cannula.
He has severe obstructive sleep apnea for which he is on auto CPAP. He has pulmonary hypertension type two and three. We plan to get AST and ALT along with TSH and CPK before initiating high-dose Atorva or rosuvastatin and to check his LDL in six weeks to get it below 70 milligrams percent within a year. We will consider adding a GLP-1 agonist if there is no family history of pancreatitis nor a family history of medullary carcinoma of the thyroid, and we'll check a hemoglobin A1C in a year. Our patient is on oxygen and we plan to check his oxygen saturation in two to three days. Our goals for his diabetes, his hemoglobin A1C of 7.5 is perfectly okay.
We would like his blood pressure to be below 130/80. If repeat testosterone levels are low, we will consider evaluating with luteinizing hormone, FSH, and prolactin. If his repeat testosterone levels are below 150, I might consider getting an MRI of the brain. We will have the nurse call him in two weeks. We will get a telemedicine appointment for the patient in about six weeks after he's had the imaging studies and the labs that we had requested for him. I would also do a PHQ-2 and if positive follow up with a PHQ-9. Another thing is, as mentioned, I would probably get an echocardiogram in about three to six months to evaluate his pulmonary pressures.
Jessica Bard:
Well, Dr Harrison. Thank you for your excellent care and guidance in our podcast today. We’ll see you next time on Multidisciplinary Dialogue Clinical Rounds and Case Reviews.
Dr Anil Harrison:
Thank you so much, Jessica, and I thank everybody and I hope this helps.