Furosemide vs torsemide
Cisplatin & Radiation Treatment (My Experience)
2024.05.14 18:40 thepurlshq Cisplatin & Radiation Treatment (My Experience)
Update post on my progress and protocols for my treatment with side effects and how I managed it all.
Now that I'm done with treatment, I hope that this can help others who may be starting the same journey and have questions. I attribute my easy time to the premeds and my mental willpower. I focus on the positives and silver linings over the negatives. You can only control one thing -- your reactions. The rest requires you to practice acceptance.
Diagnosis: Stage 2 Endocervical Adenocarcinoma Gastric Type with LVSI
Treatment Plan: Surgery (cervix, uterus, and ovaries) followed by concurrent Chemo with Radiation with a PET Scan scheduled 2 months after treatment to determine if NED or more treatment is required.
I was scheduled for 6 chemo cycles, once a week, and 28 radiation beam therapies. Chemo happened on Monday and Radiation was Monday through Friday. I had to skip Cycle 3 on Chemo only because I was hospitalized with Norovirus and my counts were too low. I still did radiation those days.
Chemo Protocol in order of meds:
Cisplatin Symptoms: This is going to vary person to person and you may get different premeds than me.
Edited to add: get a port. You will not regret it. I plan on keeping mine for a year after NED, which will require a monthly flush. It makes things so much easier, especially if you have to be hospitalized. I didn't need the numbing cream, it hurts less than the arm pokes for labs and infusions. I asked for mine before chemo and doctor didn't think it was necessary. First treatment proved it was - I had three IV's that day and I'm still suffering from the Emend infusion (not the chemo surprisingly) on my arm. Yes, its surgery but its easy. I had it in place before my 2nd chemo and it was lifechanging. I'd keep it for life it wasn't for the monthly flushes lol, my arm veins were crap to start and the more they are poked the worse they get.
submitted by thepurlshq to CervicalCancer [link] [comments]
Now that I'm done with treatment, I hope that this can help others who may be starting the same journey and have questions. I attribute my easy time to the premeds and my mental willpower. I focus on the positives and silver linings over the negatives. You can only control one thing -- your reactions. The rest requires you to practice acceptance.
Diagnosis: Stage 2 Endocervical Adenocarcinoma Gastric Type with LVSI
Treatment Plan: Surgery (cervix, uterus, and ovaries) followed by concurrent Chemo with Radiation with a PET Scan scheduled 2 months after treatment to determine if NED or more treatment is required.
I was scheduled for 6 chemo cycles, once a week, and 28 radiation beam therapies. Chemo happened on Monday and Radiation was Monday through Friday. I had to skip Cycle 3 on Chemo only because I was hospitalized with Norovirus and my counts were too low. I still did radiation those days.
Chemo Protocol in order of meds:
- Magnesium Sulfate + Potassium Chloride. Cisplatin strips this from your body, supplements.
- Emend (Fosaprepitant) - antiemetic. I had to get a port for this, it burned my arm vein and I had to use other arm for Chemo, no fun.
- Aloxi (Palonosetron) - antiemetic.
- Decadron (Dexamethasone) - steroid. It burns in your nether region, if it burns too much, ask them to push it slower.
- Lasix (Furosemide) - diuretic. Cisplatin is hard on kidneys, this is to help purge the chemo faster. Be close to a bathroom and ask nurse if you can just unplug your IV pole and go to bathroom freely vs. pushing call button -- its easier.
- Cisplatin (Platinol) 70mg (my dose). Didn't make me feel any different than the other infusions.
Cisplatin Symptoms: This is going to vary person to person and you may get different premeds than me.
- Mon (Day 1) - just the cold feeling in your veins from all the fluid infusions. You also gain like 5lbs of water weight that day. I was typically ravenous and ate whatever I wanted, the antiemetics made this possible. Be wary of constipation from chemo, it took me by surprise the first week. The other weeks I ate a few prunes on Sunday and then after chemo on Monday to help. Otherwise you won't poop for a week and be miserable.
- Tues (Day 2) - no appetite and I don't eat. Even marijuana does not work to stimulate. I'll force myself if DH forces me, but since I eat everything in sight Day 1 I'm not too hard on myself. Important to have first BM this day, if nothing then you need to start addressing. Of course I BM daily so this may not apply to you.
- Wed - Thu (Day 3 - 4) - acid reflux and indigestion. Keep some Tums handy or use pills, it doesn't really help and you get used to it. All in, better than throwing up, so take it as a win if this is the worst for you. Appetite back.
- Fri - Sun (Day 5 -7) - less side effects, should be at normal BMs, if you are not you need to address for next cycle. Very important to purge your bowels if you are constipated before your next chemo. I ended up doing Miralax my first week, I had zero BM before Sat and I could feel the pressure. The following weeks I just did a handful of prunes Sunday night after dinner and Monday when I got home from chemo. I happen to like prunes and they worked to keep me regular.
- The fatigue sets in slowly. By week 3/4 I needed 12 hours a night to sleep. Don't ignore this important rest. I adjusted my work schedule from day 1 -- from 7a to 1p Tue - Thu. I didn't work Mon due to Chemo and Fri I had to get labs done and radiation so I worked from 7a to 11am. I did this from day 1 to set the tone with my boss and ensure I had the time needed to rest even if I didn't need it. I ended up working Sat and sometimes Sun to make up for things. I am a WFH executive - right hand of CEO and in charge of operations. Helps to have a great boss pick up the slack and an amazing team who supported me every step of the way.
- Bowels get softer over time, they do not go from hard to diarrhea overnight. If you have diarrhea fast, don't ignore it or let your doctor's ignore. I thought it was the prunes week 2 that did it, no it was norovirus. They didn't catch it until I had a 102 fever week 3 and had to be hospitalized. The chemo constipation masked it during the week.
- AZO is your BEST FRIEND. Take it every day. It is made to as a pain reliever for the bladder. I missed it for a week and paid for it so bad. Do not skip this important drug. I need to keep taking it for a few weeks until the symptoms subside.
- When you go in for your initial telemetry setup for the machines, make sure you are comfortable before they start anything. The moment you lay down on the machine bed, you need to make sure you are in a good position. They used a mold on my legs and I was not in a good position so it really hurt my hips every session thereafter.
- You have to put your hands on your chest. They give a ring, I hated it. I recommend relaxing your shoulders or you'll have a hard time while they do the treatment.
- You get used to the flow. You walk into the treatment room, hop on a bed while two techs adjust you (I had x marks on both hips and belly that they lined up). Then you get a quick CT to ensure your bladder is full and you're in a good position. Adjustments are made as needed. You know when the radiation beam starts because it is the only thing with noise. Don't move until they say you can. Whole thing is 10 mins or less.
- Bladder management is the worst part. You need to have a full bladder for this and as the treatment progresses you will have a harder time determining if your bladder is full or not. Your kidneys will also work slower (I attribute to the chemo) as the weeks go on, so you'll need to drink earlier. I recommend drinking what will fill your bladder two hours before your treatment. It is easier to let of some pressure than it is to fill the bladder. Tea is a natural diuretic and is very helpful to giving your kidneys a boost. I usually drank 20+ oz of Powerade two hours before (chugging), then tea when I arrived (they had fancy machines) and this worked 90% of the time.
- Be wary of foods you eat. I did great until Week 4 when I had lots of stuff with red sauce and it caused gas. I had to pass this gas before they could do my treatment, it was a riot but you don't want your visits to be like that every day. Stay away from tomato products and anything else that gives you even mild gas outside of treatment. It is nearly impossible to pass gas with an overfull bladder.
Edited to add: get a port. You will not regret it. I plan on keeping mine for a year after NED, which will require a monthly flush. It makes things so much easier, especially if you have to be hospitalized. I didn't need the numbing cream, it hurts less than the arm pokes for labs and infusions. I asked for mine before chemo and doctor didn't think it was necessary. First treatment proved it was - I had three IV's that day and I'm still suffering from the Emend infusion (not the chemo surprisingly) on my arm. Yes, its surgery but its easy. I had it in place before my 2nd chemo and it was lifechanging. I'd keep it for life it wasn't for the monthly flushes lol, my arm veins were crap to start and the more they are poked the worse they get.
2024.04.19 21:07 ninasinparis I failed my NCLEX at 95 questions, could the quick results have been a mistake? Or failed due to a suspicion of cheating?
Hi y’all, I took my NCLEX 2 days ago and it stopped me at 95 questions. I felt good about myself cause I felt like I knew most of the questions….until now. My quick result said I failed but how possibly? I do not want to believe I failed so hard the computer had to stop me and not let me go up to 150 questions. Could the quick result be wrong? I did write non math related stuff on the whiteboard they gave me but I didn’t write direct questions. I wrote down key words to help jog my memory. For example if I was asked what position to put a patient in I would draw stick figures in those positions to make sure I wasn’t crazy. Or if it was asking about non common pharm I would write down medication with the same ending. Example Torsemide and Furosemide. Writing that down would help me figure out the medication. And I did not write down anything during the tutorial for it to be considered brain dumping. But could I have failed due to a suspicion of cheating? I will not take any chances next time and write ANYTHING down but I’m so distraught 😭😭😭😭😭
submitted by ninasinparis to NCLEX [link] [comments]
2024.04.17 16:03 arose123 4 year old Doberman heart failure - Medicine Check
* Species: Dog
* Age: 4 years
*Sex/Neuter status: Female/Spay
* Breed: Doberman
* Body weight: 36.6 kg
* History:
Talia is a 4 Yrs. 2 Mos. year old, Spayed Female Doberman who was presented to [LOCATION] for chronic diarrhea. Per owner Talia's symptoms first started in mid-October. Since coming through the ER she has not been doing well. She had a very mucoid stool after ER, which was initially improved on the probiotic. Similarly, the owner started prednisone about 11/6 due to concern of pain and not eating. By day 5 the stool was formed and she was playing, had normal mobility, eating and appeared well.Since reducing the prednisone to SID, she has had varying consistencies of stool from liguid to soft somewhat formed. When stools have less consistency the amount seems smaller and she is going about 2x daily, though increased attempts are noted when outside. When her stools are normal she was going about 2x daily. Similarly, since being on the lower dose of steroids her appetite is poor. She ate some treats yesterday, but mostly has not eaten for 2 days per owner. Various enticements have been offered including chicken,tuna, salami which she haslike though variably. Talia was seen by BP SF Urgent Care 9/1/23 where ulcerated bleeding interdigital cysts on both forelimbs, focal ulcerative lesion on the ventral rostral muzzle on exam and had presented for these lesions as well as worsening pruritus. Cefpodoxime and Cytopoint were prescribed. Skin biopsies were declined.
She was then seen byBP SF ER 10/24/23 for diarrhea, lethargy, anorexia. She recently was placed on an NSAID for hind limb pain. Temperature was 103.8, prescapular LN were enlarged and firm (FNA was fat), tense abdomen, generalized stiffness with neck pain, hooded vulva, subluxation of R hip on extension were noted. CBC noted inflammatory leukogram (WBC 22.35, Neut 19.31, mono 1.6), PIt 316K. Chemistry was normalthough glob high normal 4.4 (high 4.5) (alb 3, creat 0.7, choles 184, gluc 128). 4DX negative. In house cortisolwas 6.6. US was normal. B12 was low normal 420, Folate low 4.9 (7.7-24.4), TLI low normal (5-35), PSL low 18. She was positive for roundworm antigens, Giardia PCR, C. perf alpha toxin P C with high level genes. Her fever resolved after started Unasyn and her hypertension and pain (especially hind limbs) were controlled with analgesia. She was discharge on Clavamox, Entyce, Cerenia, Gabapentin.
He was seen 10/26/23 by BP SF Neurology where lymphadenopathy was again noted along with temp 103.2. Discomfort on mid thoracic spine was noted along with hesitance to lay and get up. Congenital spinal malformation was noted onthoracic radiographs with I D space narrowing in thorax, mid to caudal lumbar spaces, L3-L4 notable narrowed with irregular end plate lucency and sclerotic irregular spondylosis deformans. Panacur, gaba, methocarbamol, clavamox was prescribed. Joints taps returned as a predominance of mononuclear cells with increased erythrocytes ni the Lstifle (suspect contamination) with no cytologic abnormalities ni the Lcarpus and tarsus. tI was thought that DISH and/or IDD and/or discospondylitis and/or nerve root entrapment was leadingto her signs. She was then seen byDogWood 11/4/23 at which time Enrofloxacin was prescribed for possible discospondylitis along with amantadine as no improvement was noted on the abovetherapy. Her tempt h e n was 102.9 and localized T3-L3. Steroids were reserved.
Talia has been treated with i/d, fortiflora, Imodium, metronidazole for diarrhea inthe past (2020). In 2020 she had a few episodes of seeming high, panting, not wanting to use her back legs though conscious. She was seen by ER for this and was normal on presentation and drug screen negative. CBC noted mild eosinophilia 1.44 though CBC and chem was otherwise normal. She was treated with doxycycline for presumed kennel cough in April 2021.
Historical urinary incontinence, managed on Prion; anxiety, managed with fluoxetine and trazodone; hind limb pain, managed with recent Deramaxx
LEADS TO NOW: Talia was back to norm and on her meditations - Owner rushed Talia to the emergency vet on 4/10/24 because she wasn't breathing normally.
Here is the dignosis: Congestive heart failure- resolved Left ventricular systolic dysfunction - atypical dilated cardiomyopathy vs secondary to systemic disease (i.e. enteropathy ) Historical diskospondylitis, under management with BluePearl Farmington • T9-10 discospondylitis. Historical urinary incontinence, managed with Proin Historic chronic enteropathy- low folate, low normal B12
* Clinical signs: difficulty breathing (for the latest diagnosis)
* Duration: ~1.5 days
* Your general location: Michigan, USA
* Links to any test results, X-rays, vet reports etc. that you have: https://imgur.com/a/l1cT84I
Previous Medication:
Gabapentin 300mg BID, Proin 74mg BID, Probiotic SID, Prednisone 10mg EOD, Fluoxetine 60mg SID, Amantadine, Enrofloxacin 300mg SID
New Added Medication:
Furosemide 80mg tablets- give 1 tablet by mouth every 12 hours. Please ensure access to water at all times.
Pimobendan 10mg tablets -please give 1 tablet by mouth every 12 hours. Please continue her other medications as previously prescribed: Gabapentin 300mg BID, Proin 74mg BID, Probiotic SID, Prednisone 10mg EOD, Fluoxetine 60mg SID, Amantadine, Enrofloxacin 300mg SID
Question: Is there anything in the previous medication combination that could have caused heart failure? Any concerns of these medications going together? The vets keep telling me to go to one person to other to get clarity and I'm getting concerned in the level of knowledge.
submitted by arose123 to AskVet [link] [comments]
* Age: 4 years
*Sex/Neuter status: Female/Spay
* Breed: Doberman
* Body weight: 36.6 kg
* History:
Talia is a 4 Yrs. 2 Mos. year old, Spayed Female Doberman who was presented to [LOCATION] for chronic diarrhea. Per owner Talia's symptoms first started in mid-October. Since coming through the ER she has not been doing well. She had a very mucoid stool after ER, which was initially improved on the probiotic. Similarly, the owner started prednisone about 11/6 due to concern of pain and not eating. By day 5 the stool was formed and she was playing, had normal mobility, eating and appeared well.Since reducing the prednisone to SID, she has had varying consistencies of stool from liguid to soft somewhat formed. When stools have less consistency the amount seems smaller and she is going about 2x daily, though increased attempts are noted when outside. When her stools are normal she was going about 2x daily. Similarly, since being on the lower dose of steroids her appetite is poor. She ate some treats yesterday, but mostly has not eaten for 2 days per owner. Various enticements have been offered including chicken,tuna, salami which she haslike though variably. Talia was seen by BP SF Urgent Care 9/1/23 where ulcerated bleeding interdigital cysts on both forelimbs, focal ulcerative lesion on the ventral rostral muzzle on exam and had presented for these lesions as well as worsening pruritus. Cefpodoxime and Cytopoint were prescribed. Skin biopsies were declined.
She was then seen byBP SF ER 10/24/23 for diarrhea, lethargy, anorexia. She recently was placed on an NSAID for hind limb pain. Temperature was 103.8, prescapular LN were enlarged and firm (FNA was fat), tense abdomen, generalized stiffness with neck pain, hooded vulva, subluxation of R hip on extension were noted. CBC noted inflammatory leukogram (WBC 22.35, Neut 19.31, mono 1.6), PIt 316K. Chemistry was normalthough glob high normal 4.4 (high 4.5) (alb 3, creat 0.7, choles 184, gluc 128). 4DX negative. In house cortisolwas 6.6. US was normal. B12 was low normal 420, Folate low 4.9 (7.7-24.4), TLI low normal (5-35), PSL low 18. She was positive for roundworm antigens, Giardia PCR, C. perf alpha toxin P C with high level genes. Her fever resolved after started Unasyn and her hypertension and pain (especially hind limbs) were controlled with analgesia. She was discharge on Clavamox, Entyce, Cerenia, Gabapentin.
He was seen 10/26/23 by BP SF Neurology where lymphadenopathy was again noted along with temp 103.2. Discomfort on mid thoracic spine was noted along with hesitance to lay and get up. Congenital spinal malformation was noted onthoracic radiographs with I D space narrowing in thorax, mid to caudal lumbar spaces, L3-L4 notable narrowed with irregular end plate lucency and sclerotic irregular spondylosis deformans. Panacur, gaba, methocarbamol, clavamox was prescribed. Joints taps returned as a predominance of mononuclear cells with increased erythrocytes ni the Lstifle (suspect contamination) with no cytologic abnormalities ni the Lcarpus and tarsus. tI was thought that DISH and/or IDD and/or discospondylitis and/or nerve root entrapment was leadingto her signs. She was then seen byDogWood 11/4/23 at which time Enrofloxacin was prescribed for possible discospondylitis along with amantadine as no improvement was noted on the abovetherapy. Her tempt h e n was 102.9 and localized T3-L3. Steroids were reserved.
Talia has been treated with i/d, fortiflora, Imodium, metronidazole for diarrhea inthe past (2020). In 2020 she had a few episodes of seeming high, panting, not wanting to use her back legs though conscious. She was seen by ER for this and was normal on presentation and drug screen negative. CBC noted mild eosinophilia 1.44 though CBC and chem was otherwise normal. She was treated with doxycycline for presumed kennel cough in April 2021.
Historical urinary incontinence, managed on Prion; anxiety, managed with fluoxetine and trazodone; hind limb pain, managed with recent Deramaxx
LEADS TO NOW: Talia was back to norm and on her meditations - Owner rushed Talia to the emergency vet on 4/10/24 because she wasn't breathing normally.
Here is the dignosis: Congestive heart failure- resolved Left ventricular systolic dysfunction - atypical dilated cardiomyopathy vs secondary to systemic disease (i.e. enteropathy ) Historical diskospondylitis, under management with BluePearl Farmington • T9-10 discospondylitis. Historical urinary incontinence, managed with Proin Historic chronic enteropathy- low folate, low normal B12
* Clinical signs: difficulty breathing (for the latest diagnosis)
* Duration: ~1.5 days
* Your general location: Michigan, USA
* Links to any test results, X-rays, vet reports etc. that you have: https://imgur.com/a/l1cT84I
Previous Medication:
Gabapentin 300mg BID, Proin 74mg BID, Probiotic SID, Prednisone 10mg EOD, Fluoxetine 60mg SID, Amantadine, Enrofloxacin 300mg SID
New Added Medication:
Furosemide 80mg tablets- give 1 tablet by mouth every 12 hours. Please ensure access to water at all times.
Pimobendan 10mg tablets -please give 1 tablet by mouth every 12 hours. Please continue her other medications as previously prescribed: Gabapentin 300mg BID, Proin 74mg BID, Probiotic SID, Prednisone 10mg EOD, Fluoxetine 60mg SID, Amantadine, Enrofloxacin 300mg SID
Question: Is there anything in the previous medication combination that could have caused heart failure? Any concerns of these medications going together? The vets keep telling me to go to one person to other to get clarity and I'm getting concerned in the level of knowledge.
2024.03.05 20:41 Mindless_Friend8235 Why do ER vets stress euthanasia with long-term managed conditions so much?
One of our dogs (11.5 years) has advanced mitral valve disease, and has been in the excellent care of a Board Certified Cardiologist for several years. (USA)
In December, our dog had a crisis of Congestive Heart Failure. We spoke to our cardiologist who considered this routine, expected, and not a big deal in their long-term care. They advised a few days of IV Lasix therapy and went to their recommended ER. The criticalist kept suggesting and advocating euthanasia during intake, noting the cost and prognosis. We kept replying our dog's condition has been managed long-term by a board certified cardiologist, we have insurance, and we have been prepared they may have several ER trips in their final years. The criticalist replied we should consider euthanasia for cost, because they will not accept insurance and require a large deposit. We insisted on treatment. An hour later we are introduced to their head of cardiology, who looked over the case and expected a speedy and routine recovery. 36 hours later, our dog is home on a new regimen of medicine and is thriving. After a bit of analysis and adjusting the dose, our cardiologist realized there was evidence of a furosemide tolerance developing for several months, and we switched to torsemide.
In February, the same dog spiraled into dehydration and acute kidney failure after a bout of diarrhea (two bowel movements within 8 hours) after a positive cardio recheck that day. Our normal vet and cardiologist coordinated treatment plans to balance the concerns for hydration/kidneys with cardiac therapy a few days later after we had some concerns. Unfortunately they did not work and our dog needed to be hospitalized (at a different ER in a different state). Our cardiologist and normal vet strongly believed this was a survivable crisis, but the ER disagreed and kept recommending euthanasia as there was no hope. We kept our dog hospitalized for IV fluid therapy for two nights, hoping to stabilize our dog to have some positive last moments at home before our vet would make a housecall for end-of-life services. We did not want them to pass in the hospital if at all possible. The ER vets kept stressing the hopelessness of the situation and imminent death due to the renal values not declining fast enough for them. Our vet and cardiologist both still had faith, noting the IV therapy was conservative due to cardiac concerns.
We brought our dog home and coordinated end of life plans with our vet. This included two blood tests, in case they somehow survived, to see if they stabilized at all. We all (vets and owners) wanted to see some accurate third party labs done, as we did not want to make an end-of-life decision based on faulty readings or margins of error. [The renal values exceeded the machine's readability, so were computed with a dilution factor.] I requested to leave the ER with a kit to administer subcutaneous fluids, so our dog would not dehydrate. After coming home, our dog was much less stressed and interested in eating and drinking again. I administered subcutaneous shots as directed, and coordinated with our normal vet to increase/decrease as needed as the situation improved.
Our dog survived to both blood tests, which both showed continued renal improvement. Despite the declines being moderate overall, our cardio and normal vet expected them to drop significantly slower and are incredibly pleased and expect the numbers to continue to drop over the next few weeks. They both think our dog is somewhere between stages 2-3 of Chronic Kidney Disease and not end-of-life. Neither understand the rush of the ER to euthanize. We've slightly adjusted heart medication and have begun kidney treatment.
Our dog won't live forever and we know their time is limited. Through careful management of his disease by board certified specialists, he has no symptoms and should remain that way for 9-12 months when he will begin to have symptoms and we will make the quality-of-life decision.
In both ER trips, the criticalists stressed hopelessness and recommended euthanasia. Both times, days after bringing our dog home, they are running around the house, racing up stairs, and playing with other dogs in a park or on the beach. With medicine, our dog's quality of life is excellent and they are no way near euthanasia on any of the scales used in this sub.
I am still trying to wrap my head around this, and figure out how/when I can trust ER vets and when I should be second guessing them. Is this a cultural thing? Is this based on education or clinical experience? There was a tangible rush and pressure to euthanize a dog who is in a survivable crisis with a condition that can be successfully managed with long term care.
For the vets that want to know about numbers:
The normal baseline of Creat/Bun is 2.1/75 +- 15% over the past 2 years.The cardiologist measured 2.3/86 - the day of diarrhea.Five days later, the normal vet measured 6.9/140.Three days after that, the ER projected 12.8/170.Two days later the ER discharged with 7.6/180 (bun was projected, creat was readable).Two days later, our vet measured 5.4/128.Two days later, our vet measured 4.9/114.We have a renal recheck in 2 weeks.
submitted by Mindless_Friend8235 to AskVet [link] [comments]
In December, our dog had a crisis of Congestive Heart Failure. We spoke to our cardiologist who considered this routine, expected, and not a big deal in their long-term care. They advised a few days of IV Lasix therapy and went to their recommended ER. The criticalist kept suggesting and advocating euthanasia during intake, noting the cost and prognosis. We kept replying our dog's condition has been managed long-term by a board certified cardiologist, we have insurance, and we have been prepared they may have several ER trips in their final years. The criticalist replied we should consider euthanasia for cost, because they will not accept insurance and require a large deposit. We insisted on treatment. An hour later we are introduced to their head of cardiology, who looked over the case and expected a speedy and routine recovery. 36 hours later, our dog is home on a new regimen of medicine and is thriving. After a bit of analysis and adjusting the dose, our cardiologist realized there was evidence of a furosemide tolerance developing for several months, and we switched to torsemide.
In February, the same dog spiraled into dehydration and acute kidney failure after a bout of diarrhea (two bowel movements within 8 hours) after a positive cardio recheck that day. Our normal vet and cardiologist coordinated treatment plans to balance the concerns for hydration/kidneys with cardiac therapy a few days later after we had some concerns. Unfortunately they did not work and our dog needed to be hospitalized (at a different ER in a different state). Our cardiologist and normal vet strongly believed this was a survivable crisis, but the ER disagreed and kept recommending euthanasia as there was no hope. We kept our dog hospitalized for IV fluid therapy for two nights, hoping to stabilize our dog to have some positive last moments at home before our vet would make a housecall for end-of-life services. We did not want them to pass in the hospital if at all possible. The ER vets kept stressing the hopelessness of the situation and imminent death due to the renal values not declining fast enough for them. Our vet and cardiologist both still had faith, noting the IV therapy was conservative due to cardiac concerns.
We brought our dog home and coordinated end of life plans with our vet. This included two blood tests, in case they somehow survived, to see if they stabilized at all. We all (vets and owners) wanted to see some accurate third party labs done, as we did not want to make an end-of-life decision based on faulty readings or margins of error. [The renal values exceeded the machine's readability, so were computed with a dilution factor.] I requested to leave the ER with a kit to administer subcutaneous fluids, so our dog would not dehydrate. After coming home, our dog was much less stressed and interested in eating and drinking again. I administered subcutaneous shots as directed, and coordinated with our normal vet to increase/decrease as needed as the situation improved.
Our dog survived to both blood tests, which both showed continued renal improvement. Despite the declines being moderate overall, our cardio and normal vet expected them to drop significantly slower and are incredibly pleased and expect the numbers to continue to drop over the next few weeks. They both think our dog is somewhere between stages 2-3 of Chronic Kidney Disease and not end-of-life. Neither understand the rush of the ER to euthanize. We've slightly adjusted heart medication and have begun kidney treatment.
Our dog won't live forever and we know their time is limited. Through careful management of his disease by board certified specialists, he has no symptoms and should remain that way for 9-12 months when he will begin to have symptoms and we will make the quality-of-life decision.
In both ER trips, the criticalists stressed hopelessness and recommended euthanasia. Both times, days after bringing our dog home, they are running around the house, racing up stairs, and playing with other dogs in a park or on the beach. With medicine, our dog's quality of life is excellent and they are no way near euthanasia on any of the scales used in this sub.
I am still trying to wrap my head around this, and figure out how/when I can trust ER vets and when I should be second guessing them. Is this a cultural thing? Is this based on education or clinical experience? There was a tangible rush and pressure to euthanize a dog who is in a survivable crisis with a condition that can be successfully managed with long term care.
For the vets that want to know about numbers:
The normal baseline of Creat/Bun is 2.1/75 +- 15% over the past 2 years.The cardiologist measured 2.3/86 - the day of diarrhea.Five days later, the normal vet measured 6.9/140.Three days after that, the ER projected 12.8/170.Two days later the ER discharged with 7.6/180 (bun was projected, creat was readable).Two days later, our vet measured 5.4/128.Two days later, our vet measured 4.9/114.We have a renal recheck in 2 weeks.
2024.02.23 23:20 Ok_Ability_479 Home care tips for canine renal failure
Canine 11.5 years Yorkie Mix 13lbs Late Stage Mitral Valve Disease USA
Our dog has late stage mitral valve disease. They have been on cardiac therapy drugs for 4 years. They were hospitalized in December for a first episode of CHF; in January we realized the cause was developing a tolerance to furosemide (kept increasing doses) and switched to torsemide. BUN and Creat were high but normal for them at the 10 day cardio checkup (86, 2.3) . On the 11th day they started showing signs of gastroenteritis (shaking, diminished appetite) that did not clear up. Normal vet and cardiologist both thought it was GI. On the 15th day, we brought the pup in for bloodwork and the vet was convinced it was GI. I was not. Test results came back and skyrocketed - BUN is at 150, Creat is 7.
Normal vet does not want to handle primary treatment, as everything they would do is contraindicated for the cardiac treatment. They called into cardio and had us follow up.
Cardiologist (board certified) thanked vet and confirmed they made the right call in stepping back for all the right reasons. Both feel IV fluids to flush out the system are extremely likely to trigger CHF. Both think there was probably a slight GI issue that snowballed into renal failure due to a mix of diuretics and dehyrdation. Cardio had us suspend diuretics and blood pressure meds, but keep pimobenden, send us to the normal vet for a subcutaneous fluid injection. We're to encourage hydration and eating, hoping the lack of meds and moderate hydration will help him reset. If there are any signs of breathing issues, we are to slowly introduce torsemide. If there are any signs that critical care is needed, we are to rush to emergency.
Are there any hyrdation tips people have here? Are there any conditions or tests we should ensure our care team explores? Our normal vet just sent out for thyroid tests.
We know we don't have much more time with our little guy, but he has had an EXCELLENT quality of life throughout the past few months and just had a great cardio checkup. Developing a furosemide tolerance was unfortunate; switching to torsemide gave us 10 amazing days of his best health since this summer - and really made us think he would last through the year.
submitted by Ok_Ability_479 to AskVet [link] [comments]
Our dog has late stage mitral valve disease. They have been on cardiac therapy drugs for 4 years. They were hospitalized in December for a first episode of CHF; in January we realized the cause was developing a tolerance to furosemide (kept increasing doses) and switched to torsemide. BUN and Creat were high but normal for them at the 10 day cardio checkup (86, 2.3) . On the 11th day they started showing signs of gastroenteritis (shaking, diminished appetite) that did not clear up. Normal vet and cardiologist both thought it was GI. On the 15th day, we brought the pup in for bloodwork and the vet was convinced it was GI. I was not. Test results came back and skyrocketed - BUN is at 150, Creat is 7.
Normal vet does not want to handle primary treatment, as everything they would do is contraindicated for the cardiac treatment. They called into cardio and had us follow up.
Cardiologist (board certified) thanked vet and confirmed they made the right call in stepping back for all the right reasons. Both feel IV fluids to flush out the system are extremely likely to trigger CHF. Both think there was probably a slight GI issue that snowballed into renal failure due to a mix of diuretics and dehyrdation. Cardio had us suspend diuretics and blood pressure meds, but keep pimobenden, send us to the normal vet for a subcutaneous fluid injection. We're to encourage hydration and eating, hoping the lack of meds and moderate hydration will help him reset. If there are any signs of breathing issues, we are to slowly introduce torsemide. If there are any signs that critical care is needed, we are to rush to emergency.
Are there any hyrdation tips people have here? Are there any conditions or tests we should ensure our care team explores? Our normal vet just sent out for thyroid tests.
We know we don't have much more time with our little guy, but he has had an EXCELLENT quality of life throughout the past few months and just had a great cardio checkup. Developing a furosemide tolerance was unfortunate; switching to torsemide gave us 10 amazing days of his best health since this summer - and really made us think he would last through the year.
2024.02.08 19:54 Mindless_Friend8235 Is furosemide resistance known to be permanent?
Species: Canine Age: 11
We are seeing our cardiologist next week for a recheck, but I have a question until then-
After 3 months of Cardiologist/ER visits and declining health, we are finally pretty certain the underlying cause of everything is that our dog had developed a resistance to Furosemide. He has since switched to Torsemide and is doing exceptionally well now.
I have not been able to find out the following: is Furosemide resistance in dogs known to permanent or temporary (or not studied at all)? With human drugs, resistance is sometimes temporary and drugs are sometimes used in cycles to maintain efficacy. I can't find any information on canines regarding this.
Thank you!
submitted by Mindless_Friend8235 to AskVet [link] [comments]
We are seeing our cardiologist next week for a recheck, but I have a question until then-
After 3 months of Cardiologist/ER visits and declining health, we are finally pretty certain the underlying cause of everything is that our dog had developed a resistance to Furosemide. He has since switched to Torsemide and is doing exceptionally well now.
I have not been able to find out the following: is Furosemide resistance in dogs known to permanent or temporary (or not studied at all)? With human drugs, resistance is sometimes temporary and drugs are sometimes used in cycles to maintain efficacy. I can't find any information on canines regarding this.
Thank you!
2024.01.20 04:56 Pigeonofthesea8 NT-ProBNP 2,875 ng/L > BNP > 2930 pg/mL on furosemide, worsening egfr
Hi,
My dad was recently diagnosed with heart failure. Only treatment so far has been furosemide. 40 mg, then 80mg, then 60mg, then IV furosomide in the ER and now 80 again.
These are different tests and measurements - has there been any improvement?
His GP has maxed out the furosemide and said the cardiologist has to take it from here. Follow up isn’t until Feb 2. Cardiologist’s office said he’d be “keeping a close eye on results”.
Just got the lab result, it’s Friday night. The description under it says this is an “urgent” result (vs “follow up with your doctor”).
Thoughts?
Edit: his SOB is the same as two weeks ago. Feet aren’t swollen anymore. BP is ok, weight is ok.
But it’s concerning that his kidney function is way worse than it was two weeks ago, the diuretic is maxed out and his heart seems not to be improving.
I took him to one ER last week, he had high troponin twice and they let him go without treating him. Second ER, gave him IV furosemide and said his heart failure needs to be better controlled by his GP and/or cardiologist.
Enlarged ventricle, leaky valves - can medication help with these? He is not a candidate for invasive surgery because of his age.
submitted by Pigeonofthesea8 to Heartfailure [link] [comments]
My dad was recently diagnosed with heart failure. Only treatment so far has been furosemide. 40 mg, then 80mg, then 60mg, then IV furosomide in the ER and now 80 again.
These are different tests and measurements - has there been any improvement?
His GP has maxed out the furosemide and said the cardiologist has to take it from here. Follow up isn’t until Feb 2. Cardiologist’s office said he’d be “keeping a close eye on results”.
Just got the lab result, it’s Friday night. The description under it says this is an “urgent” result (vs “follow up with your doctor”).
Thoughts?
Edit: his SOB is the same as two weeks ago. Feet aren’t swollen anymore. BP is ok, weight is ok.
But it’s concerning that his kidney function is way worse than it was two weeks ago, the diuretic is maxed out and his heart seems not to be improving.
I took him to one ER last week, he had high troponin twice and they let him go without treating him. Second ER, gave him IV furosemide and said his heart failure needs to be better controlled by his GP and/or cardiologist.
Enlarged ventricle, leaky valves - can medication help with these? He is not a candidate for invasive surgery because of his age.
2023.12.10 05:58 tonyeltigre1 Hims spray, does it really work?
Does the hims minoxidil and furosemide spray actually work? I always see the results from pictures but it’s hard to actually gauge the effectiveness because the before and afters are always “short buzz cut vs. long hair” or it’s just styled way differently and the hairs are just now covering different spots
submitted by tonyeltigre1 to tressless [link] [comments]
2023.08.26 15:32 Informal-Ad4197 Fluid challenge test vs furosemide stess test??
Is there any difference between the two in diagnosis ?
submitted by Informal-Ad4197 to Residency [link] [comments]
2023.07.27 16:42 AndreMauricePicard Follow-up: Pulmonary Oedema, treated as Anaphylaxis.
Full background: 77-year-old patient. Chagas, benign tumor on dorsam column, diabetes, high blood pressure, periohal arterial disease and chronic constipation. Glaucoma. Also renal insufficiency (found it after my transport)
In treatment with: Lactulon SOS, AAs 100mg/D, valsartan 160/12h, bisprolol 2.5/D, atorvastatin 20mg/A, clonazepam 2mg, metformin 500/12, , cilostazol 100mg/D and newly added furosemide 40mg/D
After this episode already shared She was hospitalized for 7 days. angiography was performed without lesions and echocardiogram FEY 60% AO 30 LV 53 S Y PP10 mild IAO concentric LVH. She was then diagnosed with renal insuficciency and furosemide was added a 40mg/day. Also she was instructed to reduce it to 20mg if planning to walk outside home. 2 week ago come to our base, to thank us, and gift us with a cake :)
But the monday she called due a new episode of dyspnea associated with high blood pressure. (190/100). Previos Saturday and Sunday BP levels were higher, and also increasing orthopnea. Both lungs with crackles in base, and Godet edema. She only took 20mg of furosemide that day. In the EKG RBBB + Left anterior fascicular block. I just pushed 40mg of furosemide IM. Left in observation for 3 hours in our small walk-in center. Checked her again and discharged with 140/90, without crackles in both lungs.
Yesterday she was added HCTZ 12.5 in the office by their new cardiologist. I understand that also 2mg of drospirenona would be added the next week. She didn't have an appointment until the 8/21... She won't make it alive to that date, so we moved earth and sky to get a appointment yesterday. I hope that we are on the right path.
I wanted to share it because it's a very tricky and interesting case. Lots of comorbilities including Chagas Disease perhaps not sot popular for northern hemisphere. It's endemic in my country and it causes lots of electrophysiological alterations in the heart.
submitted by AndreMauricePicard to ems [link] [comments]
In treatment with: Lactulon SOS, AAs 100mg/D, valsartan 160/12h, bisprolol 2.5/D, atorvastatin 20mg/A, clonazepam 2mg, metformin 500/12, , cilostazol 100mg/D and newly added furosemide 40mg/D
After this episode already shared She was hospitalized for 7 days. angiography was performed without lesions and echocardiogram FEY 60% AO 30 LV 53 S Y PP10 mild IAO concentric LVH. She was then diagnosed with renal insuficciency and furosemide was added a 40mg/day. Also she was instructed to reduce it to 20mg if planning to walk outside home. 2 week ago come to our base, to thank us, and gift us with a cake :)
But the monday she called due a new episode of dyspnea associated with high blood pressure. (190/100). Previos Saturday and Sunday BP levels were higher, and also increasing orthopnea. Both lungs with crackles in base, and Godet edema. She only took 20mg of furosemide that day. In the EKG RBBB + Left anterior fascicular block. I just pushed 40mg of furosemide IM. Left in observation for 3 hours in our small walk-in center. Checked her again and discharged with 140/90, without crackles in both lungs.
Yesterday she was added HCTZ 12.5 in the office by their new cardiologist. I understand that also 2mg of drospirenona would be added the next week. She didn't have an appointment until the 8/21... She won't make it alive to that date, so we moved earth and sky to get a appointment yesterday. I hope that we are on the right path.
I wanted to share it because it's a very tricky and interesting case. Lots of comorbilities including Chagas Disease perhaps not sot popular for northern hemisphere. It's endemic in my country and it causes lots of electrophysiological alterations in the heart.
2023.07.20 02:09 Awaythrowabcdefg123 Dosing schedule - CHF
Hi,
My dog has CHF and is being managed with pimobendan and furosemide at the moment. He recently had an episode where he was hospitalized for two nights to get the fluids in his lungs down and his breathing comfortable again. Obviously during his ER stint, his kidney values had been elevated as priority was his breathing.
Upon discharge, we were instructed to increase his furosemide dosage (.4mL of 25mg/mL suspension, previously from .3mL) with the frequency (3x a day) kept the same. We were told to get his lab work redone to check on his kidneys. Unfortunately his kidneys were even further elevated so our cardiologist told us to lower his furosemide to .3mL 3x a day. We were to recheck 2 weeks later.
We did another recheck and although his kidney values have decreased, not significantly enough to her liking. Her next instructions were to maintain the .3mL dose but to decrease the frequency to 2x a day and to be very on top of his breath counts so that we can stay on top of adjusting his medication if needed.
I am very very good at checking his breath count and keeping him calm. I am not concerned about this aspect but I am concerned that moving back to 2x a day would let too much fluids accumulate.
My question is: is there a difference in doing .2mL 3x a day vs .3mL 2x a day? In a 24 hour period, it’s still .6mL total. I am mostly curious about the difference in terms of keeping fluids out of his lungs and if/how it will affect his kidneys (positive/negatives of the dose/frequency).
Thank you all very much! Sorry for the typos or bad grammar, I am stressed and trying to get this all out on my phone.
submitted by Awaythrowabcdefg123 to AskVet [link] [comments]
My dog has CHF and is being managed with pimobendan and furosemide at the moment. He recently had an episode where he was hospitalized for two nights to get the fluids in his lungs down and his breathing comfortable again. Obviously during his ER stint, his kidney values had been elevated as priority was his breathing.
Upon discharge, we were instructed to increase his furosemide dosage (.4mL of 25mg/mL suspension, previously from .3mL) with the frequency (3x a day) kept the same. We were told to get his lab work redone to check on his kidneys. Unfortunately his kidneys were even further elevated so our cardiologist told us to lower his furosemide to .3mL 3x a day. We were to recheck 2 weeks later.
We did another recheck and although his kidney values have decreased, not significantly enough to her liking. Her next instructions were to maintain the .3mL dose but to decrease the frequency to 2x a day and to be very on top of his breath counts so that we can stay on top of adjusting his medication if needed.
I am very very good at checking his breath count and keeping him calm. I am not concerned about this aspect but I am concerned that moving back to 2x a day would let too much fluids accumulate.
My question is: is there a difference in doing .2mL 3x a day vs .3mL 2x a day? In a 24 hour period, it’s still .6mL total. I am mostly curious about the difference in terms of keeping fluids out of his lungs and if/how it will affect his kidneys (positive/negatives of the dose/frequency).
Thank you all very much! Sorry for the typos or bad grammar, I am stressed and trying to get this all out on my phone.
2023.05.30 03:04 Bubzoluck [22 min read] Differences that Divide Us - The role of Racial and Sex based Medicine
![[22 min read] Differences that Divide Us - The role of Racial and Sex based Medicine](https://b.thumbs.redditmedia.com/drdgPEhCD0SPAHG4xgTJ_7-qFW6bk74KhycxGd2Nmmo.jpg "[22 min read] Differences that Divide Us - The role of Racial and Sex based Medicine") | Hello and welcome back to SAR! First off, I apologize for the hiatus in blog posts but had some things pop up and now I am clear! Alright off to the good stuff: For most things in life there are few reasons why one person of a particular sex or race would be more well suited to a particular job than another person of a different sex or race. Afterall, the quality of a cup of coffee would be just the same from a Black female barista with 10 years of experience as an Asian male barista with 10 years of experience. But medicine is a bit different; we do see differences because of sex or race that are important to understand, acknowledge, and factor into the diagnosis. Obviously a male isn’t going to have pregnancy on the differential diagnosis and prostate cancer isn’t a factor for female patients. The differences in Pharmacokinetics and Pharmacodynamics of a drug, a disease, or treatment can vary wildly between the sexes or between races. So today I want to look at the differences that we are only now starting to realize and the emerging role of Pharmacogenomics as the next horizon for medicine. So the big question is: you got something big in your genes or are you just happy to see me? :P submitted by Bubzoluck to SAR_Med_Chem [link] [comments] Disclaimer: this post is not designed to be medical advice. It is merely a look at the chemistry of medications and their general effect on the body. Each person responds differently to therapy. Please talk to your doctor about starting, stopping, or changing medical treatment. Pharmaco—what?https://preview.redd.it/m9y4cbtp9v2b1.png?width=747&format=png&auto=webp&s=1b116d1a0742dc8cc6bf458e684339fe3c2c34e6 Because I am a pharmacist I want to center our discussion on the drug choices and attributes influenced by sex and race but in order to do that we have to lay a foundation. The processes that move drugs from a pill into your body are broadly referred to as ADME but there is a hidden L step that is just as important to talk about as well. The lifecycle of a drug, LADME, are the five major processes that affect a drug inside the body. Let’s look:
https://preview.redd.it/5f8b8yxq9v2b1.png?width=490&format=png&auto=webp&s=64cd2ed43f824a34992bd51a7ed6ff322f4c1f70 5. Elimination - The last step in the drug lifecycle is elimination or how it physically gets out of the body. The majority of drugs leave via urine of which the kidney is responsible for that process. Having a working kidney is key for correctly dosing a drug because an underworking kidney may not eliminate the metabolized drug fast enough causing it to accumulate. There are other pathways too; fecal excretion (through biliary elimination) is another major route but some drugs can be eliminated via the lungs (such as alcohol, which is why it can be detected in a breathalyzer), through breast milk (which is why understanding drugs in pregnancy is SUPER important), sweat, saliva, and sebum. Obviously there are major differences in LADME between males and females—after all it's hard to insert a drug vaginally in a male. But now that we have a general idea of what the drug is going to be doing, let’s dive into each section and talk about the sexual and racial differences we see at each step. Liberation—”Liberty, equality, fraternity, or death; - the last, much the easiest to bestow, O Guillotine!”When we think of liberation I want you to think of two things: getting the drug out of the formulation (such as the tablet or capsule breaking down in the stomach) and where that breakdown happens. These two factors are hugely important when we think about how the drug will eventually get absorbed—after all if you can’t liberate the drug correctly then there is no chance that it will be absorbed and then be utilized by the body. First let's talk about formulations: https://preview.redd.it/1i6ih37u9v2b1.png?width=722&format=png&auto=webp&s=f86e20c6a57e892093cc05f809239e5d32dd5d75
https://preview.redd.it/87wzqtfv9v2b1.png?width=534&format=png&auto=webp&s=5823e621318faf23a995ebe62b305184ed433e20
https://preview.redd.it/xpwwknrw9v2b1.png?width=792&format=png&auto=webp&s=b9d650e79ac21e385aa2be2dcf89865c332818cf
https://preview.redd.it/cfruoc1y9v2b1.png?width=777&format=png&auto=webp&s=77c85e5cb1ffbbc95fe5c461fa06d412750a4d8b
https://preview.redd.it/5hnd2l6z9v2b1.png?width=546&format=png&auto=webp&s=22bf98592421616b1d1ceb84ee6fef5eb2518d3d
Is that a polymorphism in your pocket?Originally I was going to look at each part of LADME individually but kept running into a problem when trying to separate the drug processes into silos. While Liberation is distinct from the rest of the process, ADME cannot really be separated into its components in a way where I can tell the story efficiently. As such we will focus on the poster drugs that are significantly affected by race and sex and then talk about the larger implications in therapeutic development. Now clearly there are drugs that are used in one sex over another, for instance you aren’t going to find Atosiban used to delay labor in a male or Sildenafil (Viagra) for erectile dysfunction in a female. Now that being said they do have other uses but you get the point—so if I talk about a drug please know that I may be talking about a specific indication as well. So with that in mind, let’s jump in! https://preview.redd.it/t743qrdnav2b1.png?width=415&format=png&auto=webp&s=ab664f0523de9b7ade071ad07840698074dc1715 https://preview.redd.it/hdrinkpxav2b1.png?width=743&format=png&auto=webp&s=cc11930d2c0922801d093b2976afdb2d15df2d78 BiDil finds a home among Black patients—Hypertension, or high blood pressure, is one of the most common conditions across all races and sexes and is usually referred to as the “Silent Killer” because, well, it doesn’t hurt. Unlike liver failure or an infection, you won’t really see any symptoms of high blood pressure but after a decade of not treating it people do develop critical end organ damage: heart failure, kidney damage, liver damage, etc. Imagine that your veins are like a garden hose; if you put your thumb over the end of the hose the velocity of the water coming out of the hose increases meaning that there is more force. So if you have higher blood pressure, you have higher force hitting your organs. So the medical community has developed countless ways of lowering blood pressure to help save our organs and we can group those medications into a couple categories.
https://preview.redd.it/iqua3w32bv2b1.png?width=343&format=png&auto=webp&s=8aeed509a15f83057db180b80eaf8b70b983a16d Hydralazine vs Isosorbide Mononitrate
https://preview.redd.it/99xtjp79av2b1.png?width=424&format=png&auto=webp&s=76359060ec8bca632878ccfa135bb45120889f60 https://preview.redd.it/t2aruc4aav2b1.png?width=800&format=png&auto=webp&s=c213b5411f28486e2c2be56b7a4a7829654009a1
https://preview.redd.it/qs817v27bv2b1.png?width=570&format=png&auto=webp&s=bfb725e4bac64a0b564ac3ac9de7151b68ce3c1b https://preview.redd.it/w71a739dbv2b1.png?width=500&format=png&auto=webp&s=5fb3dd3701992dc410e32638283928e29df14859 Liver Enzyme Distribution affects Metabolism—Once a drug is in the body it needs to be deactivated and removed eventually. This process of deactivating a drug happens during Metabolism which primarily happens in the liver via the Cytochrome P450 Enzymes. These CYP enzymes are like little factories that take up a drug and make slight modifications that remove its ability to affect the body. Each CYP enzyme is best suited for certain drugs while some enzymes, like CYP3A4 and CYP2D6, are able to handle a higher percentage of drugs. You can see in the pie chart above that some enzymes are more important in metabolism than others.
https://preview.redd.it/qtt2o87ebv2b1.png?width=460&format=png&auto=webp&s=0e15a6dc5f1319aea23ec1209a47db87ec78e31b
https://preview.redd.it/d57gfgqfbv2b1.png?width=772&format=png&auto=webp&s=ff186745a84bc3cc0f651bb11ba961a56a0bfa48
https://preview.redd.it/wbvc02bhbv2b1.png?width=616&format=png&auto=webp&s=64bef947b9a5d21babaa06216b57df76c5e8f39c
https://preview.redd.it/ardo2ygibv2b1.png?width=579&format=png&auto=webp&s=f8d09c0ec32bd15dba84dace849c87e1db58e1b3
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2023.05.28 17:44 pylori pylori's Physiology Bites - Kidney function, acute kidney injury, and acid-base disorders
Welcome!
This is a series I am going to be working on where I endeavour to cover various topics in physiology intermixed with clinical pearls to impart some knowledge that doctors of most specialties and grades will hopefully find useful when looking after acutely unwell patients. Join me as we dredge through the depths of anaesthetic exam revision to answer important questions like "why do CT ask for a pink cannula", "why frusemide is okay to give in AKI", "why is hypoxic drive a bunch of horse manure" and many more. Pick up some of this material and you'll be well on your way to becoming a pernickety anaesthetist, whether you like it or not!
Questions, comments, feedback, and suggestions are both encouraged and welcome.
Although the kidney has many functions as we noted before, the easiest methods to quantify function look at the obvious: waste production. Its function is the sum of filtration through all the glomeruli in the kidneys, the glomerular filtration rate (GFR). When a substance is freely filtered through the kidneys and is neither secreted nor reabsorbed (which occur in the tubules rather than the glomeruli), the rate at which that substance is removed or cleared from the plasma can be used to measure GFR (in mL/min).
This substance is inulin and not creatinine. Because inulin isn't naturally present in our bodies, it has to be infused and then its concentration and the rate of decay measured. This is impractical clinically, so creatinine was selected as a practical alternative. The correlation between serum creatinine and measured GFR was researched and various formulas like MDRD and CKD-EPI were developed to estimate GFR (eGFR). This is why labs report eGFR as opposed to GFR. (There are also other methods to determine GFR like radionuclide scintigraphy...)
A surrogate marker we can use for the kidneys is urine output (UO). After all the end product of glomerular filtration is the ultrafiltrate which will become the urine. If there is adequate urine output despite raised or increasing creatinine levels, we can be reasonably satisfied the kidneys are actually receiving enough blood flow to get rid of waste and perform its other functions.
Note: UO <0.5mL/kg/hr is the definition of oliguria.
Definining by creatinine is a more practical screening test in most situations, allowing earlier diagnosis and intervention. UO can be monitored during the course of the day to identify patients who are borderline or not responding to treatment, may need re-evaluation of the cause, or escalation of care. This way a combination of the two can help offset the limitations of each method.
NICE guidance already exists on the diagnosis and management of AKI, most hospitals will have care bundles or even 'AKI nurses', so I'll run over a few important points.
This is a reason why renal and ICU often advise the generic "monitor I/O" rather than taking over care. We do appreciate accurate monitoring is unrealistic on the wards, but we also don't have the ability to admit everyone when few will need a specific intervention like RRT. An adequate UO to aim for is above 0.5mL/kg/hr. As AKI resolves some patients enter a polyuric phase, this will resolve but watch that they don't become hypovolaemic in the process, it may require further fluids matching what is lost.
More practically, we can work through a blood gas in a systematic fashion to help decipher the type of acid-base disturbance. Start with pH → PO₂ (always check oxygenation) → PCO₂ (respiratory component) → HCO₃⁻ (metabolic component). I've reproduced this in a simple but limited table below for reference, but this is a more intuitive flowchart to work through.
Numbers indicate primary abnormalities, arrows indicate compensatory changes. Respiratory compensation by altering ventilation occurs quickly, while renal compensation by altering bicarbonate excretion is a much slower process.
The 'opposite' of acidosis, here we see a gain of alkali or loss of acid, with impaired bicarbonate excretion required to maintain this (via chloride or potassium depletion, impaired renal function, or volume depletion).
Until next time!
submitted by pylori to JuniorDoctorsUK [link] [comments]
This is a series I am going to be working on where I endeavour to cover various topics in physiology intermixed with clinical pearls to impart some knowledge that doctors of most specialties and grades will hopefully find useful when looking after acutely unwell patients. Join me as we dredge through the depths of anaesthetic exam revision to answer important questions like "why do CT ask for a pink cannula", "why frusemide is okay to give in AKI", "why is hypoxic drive a bunch of horse manure" and many more. Pick up some of this material and you'll be well on your way to becoming a pernickety anaesthetist, whether you like it or not!
Questions, comments, feedback, and suggestions are both encouraged and welcome.
Previous installments:
- IV access, resuscitation, fluids, and the cardiovascular system
- The physiology of ageing and illness, and its impact on critical care decision making
- Respiratory failure, oxygen therapy, and gas exchange
- Reduced consciousness, intracranial events, and the central nervous system
Kidney function, acute kidney injury, and acid-base disorders
Next stop along our systems review are the mighty kidneys. I won't talk to you about Lupus nephritis or renal tubular acidosis, however I will try my best to cover some more typical things you might encounter like acute kidney injury (AKI) and drug dosing in renal impairment while trying to avoid embarrassing myself as a non-renal doctor.What do the kidneys do?
An obvious question, they allow us to get rid of waste substances in urine. They are so much more than that however, they:- Regulate electrolyte concentrations, water balance and plasma volume, plasma osmolality
- Regulate red blood cell production
- Regulate blood pressure via RAA system influencing vascular resistance
- Maintain acid-base homeostasis
- Control Vitamin D production
- Produce glucose from proteins and triglycerides (gluconeogenesis)
How do we measure kidney function?
In some respects knowing the heart or the brain aren't working is easy. Low blood pressure and infection? Septic shock. Low blood pressure + STEMI? Cardiogenic shock. Unconsciounsess or coma? Well whatever it is, it ain't working. So what about the kidneys, well we have creatinine, right? WRONG.Although the kidney has many functions as we noted before, the easiest methods to quantify function look at the obvious: waste production. Its function is the sum of filtration through all the glomeruli in the kidneys, the glomerular filtration rate (GFR). When a substance is freely filtered through the kidneys and is neither secreted nor reabsorbed (which occur in the tubules rather than the glomeruli), the rate at which that substance is removed or cleared from the plasma can be used to measure GFR (in mL/min).
This substance is inulin and not creatinine. Because inulin isn't naturally present in our bodies, it has to be infused and then its concentration and the rate of decay measured. This is impractical clinically, so creatinine was selected as a practical alternative. The correlation between serum creatinine and measured GFR was researched and various formulas like MDRD and CKD-EPI were developed to estimate GFR (eGFR). This is why labs report eGFR as opposed to GFR. (There are also other methods to determine GFR like radionuclide scintigraphy...)
What's the problem?
The estimation of the GFR relies on assumptions that are not without problems. This review covers the topic at length, however the main points are:- Creatinine is secreted, unlike inulin. As mentioned this occurs in the tubules, so changes in secretion will affect serum creatinine level despite a static filtration rate. As renal diseases progress, more and more creatinine is secreted, making serum concentrations less reflective of actual filtration.
- To truly reflect instrinsic renal function creatinine has to be in a steady state with stable generation and serum concentration. Creatinine is produced as a waste product of protein breakdown mainly from muscles. Therefore anything affecting catabolism, muscle activity, dietary protein intake, can alter this steady state. Frail sarcopenic patients will have artificially low creatinines and may not get as significant of a rise as a young muscular person in AKI.
- There has to be adequate delivery of creatinine to the glomeruli. The kidneys receive ~20% of the cardiac output, so the heart has to be pumping out effectively with healthy blood vessels, good volume and blood flow. A hypovolaemic patient with an MI may have a high creatinine despite working kidneys, they're just not being adequately perfused. Chronic diseases like hypertension, diabetes, heart failure, lead to upset of autoregulation of normal afferent (entering) arterioles, whereas ACE inhibitors and ARBs block AT-II from causing vasoconstriction of efferent (outgoing) arterioles, an imbalance can lead to renal impairment if perfusion isn't maintained, or improved blood flow and urine output if it is.
- The studies from which eGFR formulas are derived were conducted in mostly European and North American populations with elderly, black and CKD patients being significantly underrepresented. They only measured GFR a few times a year. With increasingly older, frailer, sicker patients, leading more sedentary industrialized diets and lifestyles, will the accuracy of these formulas hold up with time?
- eGFR correlates loosely with important indicators like proteinuria, fluid status, blood pressure, acidosis, anaemia, bone disease, iron deficiency, tubular function, etc. In the absence of those indicators, the elderly often have decreased GFR without increases in morbidity and mortality.
What else we can monitor?
The example of the heart earlier was misleading. Blood pressure is influenced by many factors. Septic shock is actually a high cardiac output state with low systemic vascular resistance (SVR). Patients with heart failure can have normal blood pressures despite severe systolic dysfunction and poor exercise tolerance. Blood pressure is an easy surrogate marker because determining cardiac output and SVR is invasive and complex (of course we have focused echocardiography to help us these days).A surrogate marker we can use for the kidneys is urine output (UO). After all the end product of glomerular filtration is the ultrafiltrate which will become the urine. If there is adequate urine output despite raised or increasing creatinine levels, we can be reasonably satisfied the kidneys are actually receiving enough blood flow to get rid of waste and perform its other functions.
Acute Kidney Injury
This leads us into one of the most commonly encountered entities in hospitalised patients: AKI. Let's look at the KDIGO criteria seen in the table below.| AKI Stage | Serum creatinine criteria | Urine output criteria |
|---|---|---|
| 1 | SeCr increase ≥26 umol/L <48hrs or SeCr increase ≥1.5 - 2x from baseline | <0.5mL/kg/hr for ≥6hrs |
| 2 | SeCr increase ≥2-3x from baseline | <0.5mL/kg/hr for ≥12hrs |
| 3 | SeCr increase ≥354 umol/L <48hrs or SeCr increase ≥3x from baseline or started on renal replacement therapy (any stage) | <0.3mL/kg/hr for ≥24hrs or anuria for ≥12hrs |
Definining by creatinine is a more practical screening test in most situations, allowing earlier diagnosis and intervention. UO can be monitored during the course of the day to identify patients who are borderline or not responding to treatment, may need re-evaluation of the cause, or escalation of care. This way a combination of the two can help offset the limitations of each method.
NICE guidance already exists on the diagnosis and management of AKI, most hospitals will have care bundles or even 'AKI nurses', so I'll run over a few important points.
- Pre-renal - This only means the cause lies outside the kidneys, and in at least in the early stages there is no histological change in the kidneys. In many cases like sepsis, diarrhoea, haemorrhage, there can be a relative or absolute fluid deficit and IV fluids are generally indicated. However excessive fluids can result in interstitial oedema in the kidneys, reducing the glomerular pressure gradient and so also reducing filtration. Similarly in poor cardiac output states where there is venous congestion there is a problem with the outflow of blood from the kidneys, so this is not a cause to reflexively withhold diuretics.
- Intrinsic - Here there are structural histological changes in the kidney, caused by many intrinsic renal diseases or nephrotoxic agents like aminoglycosides, vancomycin, NSAIDs, etc. If this is suspected, stopping the offending agent generally resolves AKI without needing a biopsy. Furosemide is not mentioned here as it is not inherently nephrotoxic. Acute tubular necrosis is often mentioned as a specific clinical entity, either due to nephrotoxic agents or sustained hypoperfusion from pre-renal causes. It is not a very helpful term since histological tubular damage has rarely been proven in studies, nor does it help with treatment.
- Post-renal - Obstruction may be incomplete, acute on chronic, with a normal ultrasound, no oligo/anuria, and may be associated with other pathologies like a kidney stone with pyelonephritis or sepsis. Catheters can get blocked too so don't forget a bladder scan if anuric, and obstruction can rarely be external such as by tumours or abdominal compartment syndrome.
When do I refer to renal or ICU?
Local protocols aside, advice should be sought when the patient does not appear to be responding to medical management and there may be a need for renal replacement therapy (RRT). This is often in the form of intermittent haemodialysis (iHD) on renal wards, and continuous venovenous haemodiafiltration (CVVHDF) in ICU. There are small differences in mechanism, efficacy, and indications of the many forms of RRT, the details of which aren't important for most non specialists. Generally accepted indications for RRT include:- Symptomatic uraemia - Encephalopathy, neuropathy, pericarditis. Elevated urea on its own is not generally an indication.
- Hyperkalaemia - Persistent hyperkalaemia (>6.5) despite insulin/dextrose. Severe hyperkalaemia (>8 ) with arrhythmias, requiring pacing or isoprenaline. This can occur even without anuria and should be escalated as it obviously can be life threatening.
- Severe metabolic acidosis, pH <7.1 - This will depend upon the cause and patient's condition. Patients with DKA and pH <7 can almost always quickly be turned around with insulin and fluids. Severely septic patients may not be able to tolerate medical management long enough to improve without RRT.
- Toxins or overdose - Some medications and toxins may be removed by RRT (eg, lithium, vancomycin), with specific type of RRT better for some drugs than others. This is uncommon and decisions will depend on the input from renal, clinical state of the patient, and advice from toxbase or national poisons service. A drug may not be removed by RRT but if it leads to another entity such as acidosis it may still warrant RRT.
- Fluid overload or pulmonary oedema refractory to diuretics - If patient is anuric despite diuretics then it's more likely they'll end up requiring RRT. In contrast pulmonary oedema in decompensated heart failure with worsening renal function is not helped more by RRT than by adequate diuresis.
This is a reason why renal and ICU often advise the generic "monitor I/O" rather than taking over care. We do appreciate accurate monitoring is unrealistic on the wards, but we also don't have the ability to admit everyone when few will need a specific intervention like RRT. An adequate UO to aim for is above 0.5mL/kg/hr. As AKI resolves some patients enter a polyuric phase, this will resolve but watch that they don't become hypovolaemic in the process, it may require further fluids matching what is lost.
Renal vs ICU referral
This will depend on local arrangements and acuity. Refer to renal if:- Single organ kidney failure - Normotensive haemodynamically stable patients, not septic or comorbid with poor cardiac function. The principal reason haemodialysis is intermittent because fluid is more rapidly removed therefore borderline hypotensive patients may not tolerate large volumes of blood and fluid being rapidly withdrawn from their intravascular space. I have seen patients arrest from starting dialysis!
- Unclear cause of AKI - ICU can offer RRT as a bridge, but the underlying cause has to be treated, if the cause is unclear or there is persistent renal dysfunction, this will require renal input. We refer for this from the ICU too.
- Diagnosis requiring specialist treatment - Immunosuppressive therapy for vasculitis.
- Renal transplant patients - Even with a clear cause and response to treatment, the precarious nature of immunosuppression, renal impairment and graft function mean these usually merit a call to transplant renal physicians.
- Multiorgan failure - Borderline blood pressure, high oxygen requirements, fluctuating consciousness level, coagulopathy, these patients are unlikely to tolerate iHD, but more importantly it suggests they are critically ill and may need rapid escalation of care (if appropriate) beyond what renal can provide (intubation, vasopressors, etc).
- No on-site dialysis service - In hours there may be arrangements to transfer to partnetertiary hospital particularly for complex patients. However hospitalised dialysis patients known to the renal team may require more urgent RRT than this allows. Some ICUs have the plumbing to offer dialysis (this will need a dialysis nurse however).
- Patient in extremis - ICU may be able to offer more timely input in patients needing urgent intervention especially if prior to surgery. A patient with bowel perforation and severe AKI will usually be septic and in multiorgan failure anyway, but a 70 year old with obstructive pathology may benefit from being close to theatre to offer RRT while awaiting a nephrostomy (or exchange). If it's reversible and there is somebody willing to operate, I would even dialyse a patient with a DNACPR we wouldn't otherwise admit.
Specific considerations
- AKI in heart failure
- The heart-kidney interaction is complex and works both ways (see this review). Volume status and cardiac function needs to be carefully evaluated. Seeing CCF documented in the notes is meaningless. What does their most recent echo show? What did they present with? Stable HF with reasonable ventricular function and sepsis with no signs of overload can receive fluids. Acute cardiogenic pulmonary oedema with severe ventricular dysfunction probably has AKI rooted in the decompensation of heart failure (type 1 cardio-renal syndrome) and would benefit from diuresis.
- Acute decompensated HF is usually a hypervolaemic state. Elevated right atrial pressures reduce the arteriovenous pressure gradient in the kidney leading to venous congestion, poor outflow. Inflow is also limited adding to the poor cardiac output so glomerular filtration is reduced, leading to a vicious cycle. Aggressive diuresis with furosemide reduces this congestion, improves glomerular pressure gradient and increasing filtration (as long as the patient does not become hypovolaemic). Furosemide's initial beneficial effects in venous congestion is preceded by its diuretic action and is thought to be due to it causing venodilation, reducing preload. The addition of acetazolamide may improve decongestion further.
- Creatinine rising is not an indication to stop diuresis, it may in fact signify adequate decongestion with improved patient outcomes.
- AKI in liver disease
- Like in heart failure this is a complicated topic (see this recent review). AKI is very common, occuring in up to 50% of hospitalised patients with cirrhosis. While we hear things like hepatorenal syndrome thrown around, common things being common we have to look at all the usual causes we've discussed first (so don't just throw terlipressin at everyone!)
- Pre-renal causes are most common: Discontinue nephrotoxic drugs. Look for and cover for infections and spontaneous bacterial peritonitis. Hypovolaemia from diuretics or GI bleeds, resuscitate with crystalloids and blood as needed until euvolaemic (careful to avoid overload). Albumin has been found to improve survival in patients with SBP and can be considered if worsening renal function despite resuscitation (or following paracetensis for large volume >5L ascites). Hypervolaemia from congestion (cirrhotic cardiomyopathy leading to right heart failure can benefit from diuretics, abdominal compartment syndrome from tense ascites should be drained).
- Intrinsic leaves us with tubulointerstitial causes and hepatorenal syndrome (HRS). Low fractional excretion of sodium and urine microscopy can help confirm HRS which offers a grim prognosis. Terlipressin may improve renal function at the cost of significant pulmonary oedema so regular volume assessment and avoidance of overload is paramount. RRT would only expected to be offered if waiting, or under consideration, for liver transplantation. If not, palliation will be the most likely alternative course.
- Drug dosing
- I would avoid using the BNF in renal impairment. Many of its recommendations are different than common guidelines and frankly weird. Do talk to your pharmacist (also microbiologist where appropriate), they'll often refer to The Renal Drug Handbook which is a good resource and covers scenarios like RRT. Most drugs will be dosed based on creatinine clearance not eGFR so arm yourself with an app or calculator.
- Sodium bicarbonate
- Bicarbonate infusions offer temporary extra buffering capacity, mopping up excess hydrogen ions resulting in a higher pH. This is beneficial in hyperkalaemia as a higher pH favours potassium moving intracellularly (for this reason saline is more harmful and Hartmann's more beneficial in hyperkalaemia). It also has accepted roles in tricyclic antidepressant overdose with adverse ECG findings (QRS, QT prolongation), urinary alkalinization (in salicylate poisonining, poor evidence in rhabdomyolysis), and normal anion gap metabolic acidosis (there is high cloride to replace loss of bicarbonate, see later).
- Its use outside these indications is contentious. There is no evidence of benefit in DKA over conventional fluids even if normal saline's tendancy for acidosis may slow resolution of the acidaemia in DKA. It may be actively harmful in lactic acidosis and respiratory failure as the increased pH shifts the O2Hb dissociation curve to the left, causing reduced oxygen offloading. It also results in net CO₂ production (HCO₃⁻ + H⁺ → H₂CO₃ → H₂O + CO₂) which will have to be blown off with excess minute ventilation.
- So why do ICU and renal advise it or use it themselves even with a lack of solid indications? Well, essentially it's a temporising measure. Severe acidaemia contributes to myocardial dysfunction, arrhythmias, and catecholamine resistance. In the critically ill it can be useful as a delay while you insert lines or in the hope it will avoid the need for RRT. The BICAR-ICU trial did find it delays the need for RRT and may even possibly reduce the need. I'm not entirely sold on the latter, but it can be reasonable to try if there are positive indicators like good UO.
- How? Usually available in concentrated (8.4% with 1000mmol/L of each ion) or dilute (1.26% with 150mmol/L) forms. Due to the high tonicity of the former, 1.26% is generally preferrable especially if you can or want to give larger volumes. 8.4% should be reserved for fluid restricted states and should be given slowly via a central line except in an emergency. Slow infusions help combat significant CO₂ rises and hypernatraemia (especially with 8.4%). Dosing is 1 mmol/kg which is 1mL/kg of 8.4% or 6-7mL/kg of 1.26%. For real simplicity most patients can take a 50mL vial of 8.4% or 500mL bag of 1.26%.
- Iodinated contrast
- The entity contrast induced nephropathy, better termed contrast associated acute kidney injury, is a contentious topic. There are many good reviews already on this topic.
- The evidence is from old studies using high osmolality agents during PCI. Fluctuations in creatinine may not be indicative of actual renal function and may simply reflect the underlying illness requiring a scan rather than the contrast itself. Patients are not more likely to need long term RRT.
- IV contrast with modern low osmolality agents isn't associated with AKI in patients who aren't and even those who are critically ill. There was no association in patients even with pre-existing AKI. Prophylaxis with intravenous saline nor sodium bicarbonate have been found to make a difference even in CKD patients with eGFR >30.
- The tl;dr is unless you're in cath lab or IR suite bolusing large quantities of dye arterially it is probably irrelevant. The benefit of a quality contrast enhanced scan in diagnosing and treating the patient are likely to outweigh any miniscule risk. RCR guidelines mention appropriate consent and identification of patients at risk (eGFR <40) they do not exclude the use of contrast or require hydration, at any renal function. You are the doctor, it's up to you to discuss and determine need and benefit. (It's the radiographer's job to ask, don't @ them, but they shouldn't refuse either).
Acid-base disturbances
Now it would seem we are forced to consider the fundamental concept of what acid-base physiology even is. You might have heard about strong ion difference and become lost in confusion. You're not alone. Put simply, there are two competing theories that try to explain how pH changes occur in the body: the traditional model that uses the Henderson-Hasselbalch equation to mathematically explain pH with bicarbonate, and the Stewart model that uses the concept of strong ion difference to explain why changes in bicarbonate occur. The bottom line is that these are detailed explorations of physiology more useful for bed time reading than the bedside. For the interested details can be read elsewhere.More practically, we can work through a blood gas in a systematic fashion to help decipher the type of acid-base disturbance. Start with pH → PO₂ (always check oxygenation) → PCO₂ (respiratory component) → HCO₃⁻ (metabolic component). I've reproduced this in a simple but limited table below for reference, but this is a more intuitive flowchart to work through.
| pH | PCO₂ | HCO₃⁻ | Disturbance |
|---|---|---|---|
| <7.35 | >6 | ↔ | Acute respiratory acidosis |
| ↑ | Chronic respiratory acidosis | ||
| ↔ /↓ | <22 | Metabolic acidosis | |
| >7.45 | <4.5 | ↔ | Acute respiratory alkalosis |
| ↓ | Chronic respiratory alkalosis | ||
| ↔ /↑ | >26 | Metabolic alkalosis |
Respiratory
With the topic being the kidney, I won't discuss respiratory acidosis here (see this earlier physiology bite). Acute respiratory alkalosis is due to hyperventilation blowing off CO₂. This can be due to obvious things like pain or anxiety, a compensation for hypoxaemia (eg, high altitude climbing), pregnancy (increased minute ventilation stimulated by progesterone), or salicylate poisoning (direct stimulation of respiratory centre).Metabolic
Dipping back into some physiology, we can consider two concepts that can give us more information: base excess and anion gap. The purpose of these concepts is help narrow our differential diagnosis, rather than serve as pathophysiological explanations of illness.- Base excess (BE) - This idea comes from Danish physicians during the polio epidemic where patients often experienced chronic CO₂ retention. For a standardised numerical way of gauging the degree of disturbance Siggaard-Andersen proposed BE to represent the quantity of acid in a lab that needed to be added to a solution of blood to normalise it to a pH to 7.40 and PCO₂ of 5.3. Not because the plan was to literally add acid, but this way you could easily quantify the degree of disturbance. Rather than use this concept Americans appear obsessed with the more complicated Winter's formula instead. Most blood gas analysers will calculate BE for us, often reported as standardised base excess (SBE), with a normal range of +/- 3. A negative base excess is sometimes described as a base deficit, they're the same thing.
- SBE <-3 - There is a metabolic acidosis, alone or as compensation for a respiratory alkalosis.
- SBE >3 - There is a metabolic alkalosis, alone or as compensation for a respiratory acidosis.
- Mild -4 to -9, moderate -10 to -14, and severe <-15 (same but positive values for alkalosis)
- It is especially helpful with mixed disorders or causes. A lactate of 4 doesn't explain a BE of -12 alone, are there other contributors to the acidosis? A bicarb of 30 doesn't explain a BE of +10, what else can be causing alkalosis?
- Anion gap (AG) - I have a more detailed reply here explaining anion gap. It is a theoretical number that exploits the body's need to maintain electroneutrality: we have a bunch of positively charged ions (cations) that are evenly matched with negatively charged ions (anions), and we measure some of these. When we have an excess of some anions that we don't measure like lactate this calculated number rises because one of the measured anions (bicarbonate) drops to compensate to maintain electroneutrality. Like BE, most blood gas analysers will calculate AG for you.
Metabolic acidosis
Symptoms are non-specific, with the most obvious being hyperventilation for compensation. In severely acidotic states (pH <7) seek early ICU help. Awake patients will hyperventilate sometimes down to PCO₂ <2 which can dramatically increase work of breathing. Initiating invasive ventilation in this stage or patient fatigue can be very dangerous if hyperventilation isn't maintained, the acidosis can worsen and precipitate cardiac arrest. Hypotension from vasodilation and reduced cardiac contractility can occur, as well as arrhythmias, confusion, delirium, coma.- High anion gap metabolic acidosis - The presence of unmeasured anions including: lactate, ketones (diabetes, starvation, alcoholic), salicylates, formate (metabolite of methanol), oxalate and glycolate (metabolites of ethylene glycol), other toxins.
- Normal anion gap metabolic acidosis - Losses of base (bicarbonate loss in GI tract via high ouput ileostomy or diarrhoea, renal loss via acetazolamide) or excess of acid (renal tubular acidosis, hyperchloraemia, adrenal insufficiency).
- Pitfalls: Albumin is an unmeasured anion, so low albumin can mask a high anion gap. Albumin corrected formulas have been developed. Similarly excessively high unmeasured cations like magnesium, calcium, and even lithium, can also lower the gap.
Metabolic alkalosis
Despite metabolic acidosis being the usual focus, metabolic alkalosis is actually the more common abnormality of the two in hospitalised patients and is frequently seen as a mixed disorder (like as a response to prolonged CO2 retention as seen in mechanically ventilated patients). In severe states it can lead to delirium, seizures, obtundation, arrhythmias.The 'opposite' of acidosis, here we see a gain of alkali or loss of acid, with impaired bicarbonate excretion required to maintain this (via chloride or potassium depletion, impaired renal function, or volume depletion).
- Gain of alkali - Iatrogenic from bicarbonate infusions, citrate in transfused blood.
- Loss of acid - From the kidneys via diuretic therapy, or mineralocorticoid excess, hypokalaemia. From the GI tract by vomiting especially with pyloric stenosis or obstruction as there is gastric acid loss (with chloride) only, laxative abuse diarrhoea.
Conclusion
This is another large topic where there was plenty to talk about. I had to cut down the scope significantly as it rapidly spun out of control, however I thought the nuances deserved a detailed writeup. Nothing is ever absolute so don't take any of this as incontrovertible evidence of the incompetence of a hated colleague (or their brilliance)! It will hopefully have given you some ideas to think about and research further when you see patients with AKI yourself.Until next time!
2023.03.22 23:47 MLJ21 Furosemide vs Fluids
Just wanted an update on the age old conundrum on which treatment would be best if you had a patient that was fluid overloaded but has really low BP?
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2023.02.10 13:12 hswapnil Disappointing Diuretic trials on NephJC
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2023.02.06 15:58 KamKalantar Mortality Similar With Torsemide, Furosemide for Patients Hospitalized With Heart Failure
 | submitted by KamKalantar to u/KamKalantar [link] [comments] |
2023.01.24 19:14 qwaszz2 Need a safer alternative to furosemide
My dog with heart, liver and kidney disease was prescribed furosemide because she was coughing a lot due to her heart condition and buildup of fluid in the lungs. Since she's been on it her coughing has gotten much better, but her appetite has been low/ being a picky eater, and her breath started to smell really bad. I believe that the furosemise might be causing damage to her kidneys. I'm hoping there is some other safer alternatives I can try that aren't as bad on her kidneys. I saw that there was another option called torsemide online but I'm not sure if it's any better for kidneys.
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2023.01.24 18:51 anonymous-shad0w Mortality Similar With Torsemide, Furosemide for Patients Hospitalized With Heart Failure
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2022.09.07 17:55 Minimum-Designer-305 Feeling better.
I was in the hospital last week undergoing an intravenous diureses because I was retaining so much fluid. When I left they put me on Furosemide 40 mg three times a day. I switched to the Torsemide I have because I felt like the Furosemide wasn't working. I have lost about 28 lbs of fluid since going to the hospital. I'm eating little to no salt, lota of fruits, veggies, grains. I could barely move a little over two weeks ago, but I'm feeling much better! My EF is at 40%.
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2022.05.14 21:47 Nor_Wester Heart Failure Questions
- Species: Dog
- Age: 12
- Sex/Neuter status:Female, spayed
- Breed: Leavitt Bulldog
- Body weight: 70lb
- History: Has been in heart failure since mid Feb
- Clinical signs: Acites
- Duration:3 months
- Your general location: PNW
She got the 1st one at 9PM last night. She seems to have peed more, but I woke up to her dry heaving this morning, has no appetite except for treats and seems sleepier than usual. I've read that if taken with food it may relieve the nausea, but I don't know if I should with the dry heaving appetite loss and tiredness that it caused. Also, I read today that Spironolactone shouldn't be taken with Enalapril? And why would we keep her on the Furosemide when it wasn't helping at all with fluid loss? Wouldn't switching her to Torsemide or another loop diuretic be a better course?
eta the spironolactone is once daily not twice.
2022.04.30 17:33 GummyOblongata furosemide vs spironolactone
Hello, I am misunderstanding the difference between furosemide and spironolactone as treatments for CHF, here is my understanding:
I know furosemide and spironolactone are diuretics.
Furosemide is the number drug used to treat CHF, it is potassium losing so, pee out potassium, retain sodium and water.
Spironolactone is potassium sparing so, retain potassium, pee out sodium and water. Spironolactone directly blocks aldosterone. Without aldosterone being blocked, sodium and water would be retained and pee out potassium=increase BP=make things bad for individuals with CHF. This part makes sense to me.
However, what is furosemide directly blocking and how does it helping people with CHF if it retains sodium and water?
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I know furosemide and spironolactone are diuretics.
Furosemide is the number drug used to treat CHF, it is potassium losing so, pee out potassium, retain sodium and water.
Spironolactone is potassium sparing so, retain potassium, pee out sodium and water. Spironolactone directly blocks aldosterone. Without aldosterone being blocked, sodium and water would be retained and pee out potassium=increase BP=make things bad for individuals with CHF. This part makes sense to me.
However, what is furosemide directly blocking and how does it helping people with CHF if it retains sodium and water?
2022.04.13 07:01 ije912 Gained 18lbs in 2 weeks. No one knows why.
In May 2021, I (23 yo F, 22 at the time) very suddenly gained 18lbs in 14 days. My eating habits didn't change. I was the same size for almost 9 years. I weigh myself everyday and saw the gain every single day. I was finally able to get in to the doctor and they gave me furosemide. I was given a 4 day supply and lost 10 of the 18lbs gained. After I ran out, I had to wait 3 days for a refill. In those 3 days, I gained 7 of the lost 10lbs back (15lbs above my normal weight.) I was continued on furosemide, gradually increasing the doses until the end of July. At that point I was still gaining and now 20lbs above my normal weight. At the end of July they switched me to torsemide which I'm still currently on. I've seen my rheumatologist, cardiologist, gynecologist, a nephrologist who flat out told me that he didn't know what was wrong with me, suggested I try to stop taking the diuretic following with "if 4 months from now you're 200lbs we'll know it isn't salt and something else is going on" 🥴, and a dietician since my rheumatologist suggested it could be a sudden drastic slowing of my metabolism that is causing the water retention. Got the metabolism checked and it's faster than a normal person. Every day I take the torsemide and will drop as much as 5lbs in 2 hours. By the next day, I'm back up to where I started. My normal weight is 140lbs and I've been sitting at 160, some days a little more for months now. Endocrinology refuses to see me because my thyroid is normal even though i'd like more hormones tested. Gynecology tested my testosterone, estrogen, and progesterone. All normal, but I'm on birth control so it could have swayed the numbers. Note: I was not on birth control when all of this started. I had started no new medications at the time this began. No changes to eating habits, in fact, when I saw that I was gaining, I reduced my eating in fear. Hepatology doesn't want to see me because my liver numbers are showing normal, however, non-alcoholic fatty cirrhosis of the liver runs in my family, and has killed 2 of my cousins, and almost killed my mom. She had a liver transplant in 2019. You'd think that'd be reason enough to see me but I guess not. As for my medical history, my biggest issue is mixed connective tissue disease, but I do also have gastroparesis, atrial flutters, and vestibular migraines. I'm just really tired of feeling this way. It took me 2 years to get diagnosed with mixed connective tissue disease and the only reason why was because I did my own research and asked my dermatologist to test me for lupus. But this? I can't find anything on this, which is why I'm reaching out here. I know it may sound kind of shallow but not only do I feel just a constant state of "meh" but it's really doing a number on my self-esteem. Like I said, I was the same size for almost 9 years. Literally most of my clothes I've had since I was 14/15. If you have ANY idea as to what might be going on, please let me know, because every doctor I see is at a loss, and so am I. Thanks in advance. Age: 23 Sex: Female Height: 5'0.5" Weight: 160lbs Race: black, white, native american Duration of complaint: 11 months Location (Geographic and on body): KS, USA. Entire body Any existing relevant medical issues (if any): Mixed connective tissue disease, gastroparesis, vestibular migraines, atrial flutters, ovarian cysts Current medications (if any): hydroxychloroquine, nortriptyline, torsemide, potassium cl, vitamin d2, cetirizine, montelukast, famotidine, estarylla, xolair injection. All daily aside from d2 (once a week) and xolair (every 28 days)
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