Jimmy's Lump Seems to be NON CANCEROUS Lipoma

Pathology Report:

"Jimmy Stewart's mass is thought to represent an angiolipoma. Angiolipomas are a variant of a lipoma.
Lipomas are benign connective tissue tumors composed of histologically normal adipose tissue. It has been
postulated that lipomas may represent regions of nodular hyperplasia or altered lipocyte metabolism
rather than true neoplasia. Because lipomas have no defined microscopic borders, gross inspection at the
time of surgery is often a better indicator of completeness of resection than microscopic examination.
Development of multiple lipomas is common, and close observation for additional masses would be prudent.
Surgical excision is typically curative.

 A vascular derived neoplasm was considered, but is less favored at this time. Additional recuts and
 re-trims to further characterize the lesion are pending...

  HISTOPATHOLOGIC DESCRIPTION:
  The specimen consists of multilobulated nodules of well-differentiated adipocytes supported by modest
  bands of fibrocollagenous tissue that occasionally are partially encapsulating the nodules. There are
  multifocal random branching vascular structures within this mass that are interspersed among lobules of
  mature adipocytes. Individual adipocytes have abundant cytoplasmic lipid and small compressed nuclei.
  Mitoses are not seen. Inflammation is not present..."

Jimmy CT Shows Lung Issues/Stomach Hernia, etc. Skin Lump Well Defined

There's so much going on here. I've not had a chance to stop and write-between cats, house issues, garden, personal, etc.

Lizzie-doesn't want to eat, isn't feeling well lately, was in for blood work and scans in April and has approaching CKD. We are feeding her renal foods, fluids, extra vitamins, etc. And Mirtazapine once a week and very little of it BECAUSE of the complications long term use had on Katharine (see posts December/January.) But we are hand feeding her daily three times a day and her weight is stable at 11.3 lbs. Some days she eats well on her own but not all. I want her to stay over 11 lbs because when they get down to 10 or less, they become weak, with less fat and muscles which is what we saw with Katharine.

Jimmy-as I posted in March, had two biopsies of his back lump and the second one came up possibly cancer. We had a CT in early May and THAT report came up with---a possible lung issue AND a stomach hernia and other issues. The lump? Smaller than in March and well defined and NOT spreading. SO-the CT specialist thinks it's likely not cancer but needs to be removed and tested to know for sure. We were supposed to remove it this week BUT NO ONE CAN TELL ME ABOUT THE CT REPORT and if anything is serious. The vet hospital sends them out so there's NO ONE to talk to. Our state's vet school is without a rad/onc/CT/MRI specialist since February so no one there can discuss it with me. No one else in the area will read someone else's CT unless MY VET sends it to them. AND MY VET hasn't yet despite me requesting it a week ago; AND the surgeon to remove the skin lump still hasn't called me to discuss the CT report and if there's an issue to resolve before he has surgery. His cardiologist said she can't see anything of concern on the xrays from March and feels the CT report is too vague and to continue removing the skin lump to test for cancer. BUT if the lung issue is concerning, then he can't have surgery or daily intubation for radiation treatment on the lump area if it is cancer.

I'm worried about either waiting to find out more about the lung-but where, when, who??-or risking surgery now and having something go wrong. Or waiting to remove the lump and what if it's cancer but not ACTING like cancer? And then waiting spreads it?

The CT report:

"Thoracic CT-
In the right caudal lung lobe ventrally there is an irregularly marginated, ovoid soft tissue attenuating structure, measuring approximately 2.9 x 3 mm. (VERY SMALL) This is closely associated with vessels and an airway. On the dorsal reformatted image, this appears to be associated with a curved vessel. This structure is less discrete and poorly defined on series 2, the initial scan.
There is patchy groundglass appearance within the left cranial and right mid ventral pulmonary parenchyma.

...On the second scan, the pylorus of the stomach is displaced into the caudal thorax and there is esophageal distention. There is adjacent poorly defined soft tissue attenuating material, not identified on the initial scan.

...Sternal lymph nodes are mildly enlarged with homogenous enhancement...

CONCLUSIONS:
Solitary ovoid pulmonary structure. Given that there is only 1 structure, this could represent a granuloma or neoplastic nodule, however, on the dorsal reformatted image, this has a curvilinear appearance, therefore, this also could represent a curvilinear vessel which has a nodular appearance on the transverse images.
Mild sternal lymphadenopathy.
Chronic lower airway changes. (WHAT?? Serious?)
Sliding hiatal hernia."

Jimmy

Elizabeth

Discussed Necropsy with Pathology-Getting Tox Screen

I talked to the pathologist who did Katharine’s necropsy. There’s no one specific thing that happened that led to her death. Except her pancreas wasn’t doing well. Two weeks before everything seemed OK and stable. There are a lot of things we cannot see with ultrasound, x-rays or bloodwork. You can only see them once there’s a necropsy, and you see them under the microscope. The same thing with her heart. She had lesions in her heart, the myocardial fibers disarray that they described in the necropsy means that she had lesions. This disrupts the heart’s signaling that helps it beat properly. The heart got worse with the stress from whatever was going on with her liver and pancreas that led to her death. And what happened to the heart probably created the clots that they found in the vessels of her lungs. So she died of liver and pancreas failing that upset the heart that led to clots in the lungs that meant she couldn’t properly breathe. It was a cascading effect. But what caused it initially maybe the pancreas. Which means that no matter what you do to protect them, if the pancreas gets upset, it will lead to a cat’s death. We saw this with Baby. 

There is no reason that they found in the brain for the neurological issues that she had. I can only describe it as if she had Parkinson’s disease. She had this odd twitching that was going on in her face for the last couple of months and her front right leg would shake or vibrate, depending on how she was sitting or sleeping.

They are doing a tox screen. That will take two weeks. 

Katharine's Vet Gives Me the Cause of Her Death

The necropsy doesn't offer a definitive cause of death. I posted the necropsy in the previous post.

And there are things not addressed. I'll have to call them Monday. But her vet read the report and said she died of (which is not listed as a cause in the report but she surmised the cause by the descriptions in the report:)

(DIC) "Disseminated intravascular coagulation (DIC) is a hematological syndrome characterized by the activation of intravascular coagulation resulting in excessive fibrin formation and simultaneous consumption of coagulation factors and platelets resulting in severe hemorrhaging."

She had too many clots (fibrin) in her blood vessels and organs, and especially in her lungs leading to blood loss and oxygen loss because nothing could circulate; this causes damage to all organs. This led to further organ failure including heart, lungs, liver, pancreas, kidneys. And even the thyroid showed inflammation responses to the process.

We knew she had mild CKD and her blood values had been high normal and stable TWO WEEKS before her seizure. Her cardiology report TWO WEEKS prior said that her heart disease HCM was moderate and stable from last September's checkup. Her liver and pancreas had made her sick in December, and we believe she had been getting sick since November. We had been hand feeding her all through December and January and she had seemed stable the week before she had her seizure.

Her vet believes the last seizure was caused by the underdiagnosed liver and pancreas disease (even though blood work TWO WEEKS before showed mildly elevated results and her ultrasound showed mild issues with both organs.) Apparently, severity of liver and pancreas disease cannot be accurately detected until they blow up, which is what happened after her seizure.

So, seizure caused the dominoes to fall; or the game of Jenga was being played internally and something became elevated/declined to function properly and caused her seizure which then increased the decline of her organs.

Her vet says that she was dying Saturday night/Sunday morning and that the reason she couldn't breathe wasn't because of the small amount of fluid in her lungs at death but because of the clots and lack of oxygen in her body that made breathing impossible.

I'm glad she was home when she died, that I had her bundled up in bed with me and my arm wrapped around her.

This is Katharine a few months ago, doing what she loved to do-climb up onto me, cuddle up against my head, then CHOMP DOWN on my hair.

Katharine Died Feb. 4, 2024

I hadn't realized that I had not posted her death. She died of respiratory failure. She had fluid in her lungs and however that worked, her heart stopped. We were going to give her oxygen and take her to the ER but she died before we could leave the house. 

Katharine Hepburn 

She had gone to the ER after her seizure January 27; then to the vet hospital January 28. She was there until Wednesday Jan. 31 when she came home. She was weak, couldn't-and never did-cry or make a sound. She could barely walk. The hospital said they didn't know why and that was that. We nursed her, fed her, and she could use the litter box but wouldn't eat on her own. She finally drank water Friday. But Saturday she was breathing heavily. The ER withdrew fluid from her pleural cavity-pleural effusion-but could not account for cause. She went back that evening at 9 pm but they said there was more fluid but not enough to risk removing because it was too close to the heart. Her breathing worsened over night. I should have taken her back about 2 a.m. when her breathing rate was 48 and she had this vague expression and did not easily respond to touch or speech. I had her bundled up in a blanket next to the radiator because the ER said her body temperature was dropping. She woke me at 5:30 trying to move and I picked her up and put her into bed with me. She did not try to move. She seemed to be unaware of me. She was still breathing heavily. She woke me at 6:30 with sharp, shallow sounds but still unconscious. I should have taken her then to the ER. I hesitated. I don't know why. Then it slowed about 7:15. That's when I got my husband and we were helping her when she stopped breathing. I will never again let that happen. Yes, she was likely dying but not being able to breathe must have been uncomfortable.  

We took her body for a necropsy later in the day. We received the report today, February 23, 2024. The report is inconclusive. Many things were wrong but nothing to account for the pleural effusion. No heart attack. No brain tumor. No accounting for weakness or neurological issues she had been having. No real reason for liver failure. Or why her heart stopped. She had 30ml of fluid in the pleural cavity-two tablespoons. That would have made breathing hard. But not enough to stop breathing-or so vets believe. 

We are going to request a tox screen as the pathologist suggested. And I'll speak to them next week about any other tests. 

NECROPSY

Gross Description

A 4.1kg spayed female cat was necropsied on 2/5/2024. Autolysis was mild. The animal had moderate amounts of subcutaneous and visceral fat, and had an overall body condition score of 6/9. Scant red-tinged fluid stained the fur around the left nares. The abdomen and left forelimb were shaved, and there was a small puncture wound over the left cephalic vein consistent with venipuncture. There was also a shaved region over the left side of thorax with needle puncture along with mild associated subcutaneous dark red hemorrhage. There were approximately 30ml of transparent, red tinged fluid ni pleural cavity. The lungs were diffusely mottled shades of dark red. The heart weighed 17g and the left and right ventricular free wals respectively measured 8mm and 3mm in thickness. There was a slightly enhanced reticular pattern. The left thyroid gland was dark purple, and enlarged measuring 2cm x 1cm x Icm; there were 3mm in diameter fluid filled cysts at the cranial and caudal ends. There were 3 blue, 1cm in diameter, spherical capsules in the stomach contents. No other significant lesions were observed.

Comments

Overall, the described changes are mild and likely incidental, or are related to clinical treatment or diagnostic procedures. The enlargement of the left thyroid gland may suggest thyroid hyperplasia or a benign tumor. No lesions to suggest any other specific underlying disease process were observed. 

Microscopic Description

Representative routinely stained sections of brain, heart, lung, spleen, liver, kidney, tongue, esophagus, stomach, intestines, pancreas, urinary bladder, adrenal gland, thyroid gland, haired skin, lymph node and bone marrow were examined. Autolysis was mild.

In the left ventriculum of the heart, the cardiomyocytes were often arranged in abnormally intersecting patterns and there was variation in myofiber size. Multifocally, the myocardium was replaced by moderate amounts of fibrosis. In the lung sections, the small pulmonary vessels were occluded by fibrin thrombi.

In the liver sections, there were mild multifocal centrilobular areas of hepatocellular necrosis, characterized by loss of cellular details with retention of the architecture or loss of hepatocytes and replacement by hemorrhage. There was moderate Ito cell hyperplasia. In the pancreas, there was mild focal infiltrates of degenerate neutrophils in the pancreatic parenchyma. The peripancreatic adipose tissue was extensively replaced by amorphous basophilic to amphophilic material mixed with degenerated neutrophils, consistent with saponification.

Multifocally in the kidney section, there were mild infiltrates of lymphocytes and plasma cells in the interstitium. Rare thickened Bowman's capsules were observed. The thyroid gland were moderately hyperplastic and there was a large cyst which contained high amounts of homogeneous eosinophilic fluid in the center of the thyroid. No other significant lesions

were observed.

Morphologic Diagnosis(es)

Heart: Moderate multifocal myocardial fibrosis and myocardial disarray

Liver: Mild acute multifocal centrilobular hepatocellular necrosis

Pancreas: Mild acute neutrophilic pancreatitis with severe peripancreatic fat necrosis

Lung: Mild pulmonary thromboembolism

Thyroid gland: Moderate hyperplasia with cyst

Comments

The findings in the heart are most consistent with hypertrophic cardiomyopathy (HCM), which is the most common type of cardiac disease in cats and is a common cause of sudden death. The changes in the liver may be secondary to the cardiac condition but given the centrilobular pattern, a toxic insult cannot be completely ruled out. 

The fibrin thrombi in the lung can be secondary to the heart condition or pancreatitis which can lead to disseminated intravascular coagulation (DIC). This cat also had thyroid gland hyperplasia, but this is likely non-functional and considered as an incidental finding. The findings in the kidneys are mild and likely an incidental finding as well. No further

testing is currently pending.

Katharine's Health History Since November and Possible Causes

Presents with:

• Inability to eat enough on her own.

• Physical weakness, inability to climb without stumbling.

• Sometimes shaky after taking Mirtazapine-drug interaction? Low glucose/pot; hyper/hypo? 

• Exhibits leg and facial twitching.

• Mirtazapine no longer has the anxious/eating affect; does not cause her to want to eat; not acting long term for three days.

• Mirtazapine didn’t work well with Benazepril or Gaba or Cerenia to help her eat. Was made weak         on benazepril; improved after ceasing.

• Became weak on gabapentin. Improved after ceasing.

Contraindications that may cause issues for Katharine:

• Gabapentin is contraindicated to Mirtazapine. Made her weak, not eat?

• Gaba is contra to phenobarbital. Made her weak? (Side effect for humans-weak, disorientated, etc.)

• Mirt is an antidepressant. Made her weak?

• Mirt-processed in liver/renal. Can cause ALT elevations, hepatic injury. She has had increased levels this past year.

• Mirtazapine and Cerenia do not work well together for her. Cannot be given the same day.

• Antihistamines contra to phenobarbital.

• Steroids interact with phenobarbital.

• Chronic use of Mirtazapine drives up phenobarbital levels-we saw this in her blood count in December. We saw a decline when we ceased Mirtazapine in January after a month of not taking it. 

History October-December 2023:

September

• Weight September at home-10.2 ½ 

• 9/13/23 cardio exam showed heart disease increased to 1.76. Put on Benezapril and Plavix. 

• But that made her weak immediately. She stopped eating as much. 

October

• Not eating became worse in October. Weight down 10/4/23 to 9.12 at vet.

• By 10/9/23 noticed that Mirtazapine is not making her eat as much, does not have the same effect. 

• Feeding more AD by hand 10/16/23 at 6-9 ml twice a day. 

• Cardio said to cut Benz to once a day 10/16/23. 

• 10/19/23 Mirt began not working well at all. Effect lasted about two hours. 

• She was appearing weaker, unable to stand straight and walk, and seemed tired and uncomfortable. 

• 10/20/23 cardio said to give her Atenolol BID and stop Benz. 

• Began feeding AD three times a day at 9 ml. each time. 

• Tried Cerenia and Mirt together not working well. Better when we alternate days. 

• She has trouble climbing and stumbles on stairs, and struggles with cat tree. 

• Begins to exhibit shakiness and twitching in body and head. Front legs begin to slide around when she sits and stands. 

• 10/22/23. Eating very little on her own at this point. 

• Finally by 10/26/23 she responds well to Mirt and eats well on own. Hand feed evenings only. 

• 10/27/23 weight is 9.12. 

• 10/30-31 eats on own, hand feed 9ml AD evening only.

November

• By 11/3/23 Mirt is working as normal-she eats all day long, and appears to eat all week well enough. Continue hand feeding AD evening.

• 11/11/23 weight still 9.12.  Continues through the month. 

• She is stable enough physically but not strong. 

December

• 12/3/23 wonder if lack of strength is reaction to arthritis and if should start gabapentin as previously discussed. 

• Began gaba 12/3/23 at .1ml of 50mg/ml strength. She appears to walk stronger and to stand straighter with it after receiving it in the morning. She begins to spend each day playing with catnip toys and rolling around. 

• But slowly over time, this decreases. By 12/13/23 she is appearing weak, tired, run down again. Not eating as much. Stops playing with toys, not as vocal or alert. Mirtazapine isn't working with gaba.

• Stopped gaba 12/15/23. 

• 12/16/23 weight down to 9.9. 

• 12/17/23 too weak to climb cat tree. Can’t climb shorter towers. Is very weak. Won’t eat. Not vocal. Shaky. Twitching more. Checked heart rate-150; BR seemed normal. 

• 12/19 Added corn syrup to AD to combat weakness and twitching-thought low on glucose. Increased potassium a bit more (Renal K gel.) Adding glucose seemed to backfire (sign of pancreatitis?) She was even weaker and would not eat anything. 

• Reviewed Dr. Miller’s October scan report and read about pancreatitis. Discovered it could be her liver and/or pancreatitis that is flaring up. 

• 12/20/23 began ½ Cerenia each day. 

• Asked for Hills ID from Cat Clinic and began hand feeding her that 9ml three times a day. Also fed her tunajuice 9ml three times a day. Tried to get her to eat tunafish. 

• Added taurine pills. 

• By 12/21/23 began to nibble on tunafish on her own. Continued hand feeding ID and tunajuice. 

• *Noticed her face and eyes twitching as if she can’t close them and the lids are blinking rapidly. Her front legs twitch under her for a few minutes. 

• 12/23/23-12/27/23 each day wakes up perky, walking fast down the hall, eating food overnight, very vocal, able to climb pet stairs, regular stairs, and cat condo. Then after her morning meds, quiets down; after hand feeding quiets more; after eating breakfast-which she is eating more of on her own, she quiets even more. Appears weaker and more tired by the evening. Continue to hand feed ID and tunafish juice and tuna that she eats on her own. She began eating dry food and dry treats during this week, also. Has more twitching in the evening. Breathing rate appears higher in the evening-CHF or heart or response to weakness and not eating or to being hand fed?

• Is receiving Forta Flora. Did not eat the Visibiome probiotic or Biome food.

Weight 12/22/23 at home 9.5

• Saw Dr. Miller 12/28 ultrasound gastro scan; pheno too high at 37; decreased pheno to ½ tab.

-Is mirtazapine driving up pheno level? Studies shows it can.

• Continued hand feeding ID four times a day, letting her eat what she would. 

• Continued to be weak.

January

• 1/1 Still hand feeding ID; she’s not eating well enough on her own. 

• Continues to do well in the a.m. when she wakes, and to decline in energy as the day progresses.

• 1/3-used ear drops and eye drops-ears full of black wax. Used ten days until 1/14.

• 1/4 began 75mg magnesium and 25mg potassium extra daily in a.m.

• 1/5 her weight at home is 9.3 ½.

• 1/5 began baytril. Perked her up a bit.

• 1/7 began cypro ¼ and she began to eat some on her own. Ate Fancy Feast and tuna.

• 1/8-1/10 She continues to be hand fed but begins to eat more on her own. More perky and alert also. Eats Fancy Feast and tuna.

• 1/10 weight at home is 9.5 

• 1/11 Sees cardio, heart is fine, not related to issues of inappetence. She does not eat when she gets home. Declines to eat on her own. We increase feeding PO of ID. 

• 1/11-14 We hand feed ID and offer tuna but not Fancy Feast. 

• 1/15 She perks up and begins to eat some Fancy Feast on her own and we feed ID.

• 1/16 Not eating well on her own, only a few bites of dry food and tuna. We continue to hand feed.

• 1/17 sees vet for tests: PLI, cbc/chem, bile acids, pheno. Pheno level down to 14 now that she's off mirtazapine-need to increase pheno again. RBC low, liver values high, kidney values creeping up, etc. 
•  She seems to do well with Hills ID and tuna; then begins to eat more food on her own of Fancy Feast and dry gastro fiber food; then goes into a decline. 
• Week of January 23 she was eating well on her own, stronger, playing with toys, able to climb and walk well. Seemed stable and that our schedule and process was working.
• Then she seizured Saturday January 27. Took her to the ER.

Possible causes of issues:

Her calcium is high.  Hypercalcemia can cause tremors and twitching. Inappetence. Increased thirst and urination.  Overall weakness. (Kidney stones, blockages.)

*These symptoms are also pancreatitis, heart disease, medications, high pheno, low pot, dehydration, lower calories/nutrition. 

-Caused by CKD, cancer, other issues, taking too much calc, parathyroid-leads to too much PTH. Addison’s disease-hypoaldost and low glucorticoids produced-lethargy, not eating (how to test?), caused by dehydration. (Aldosteronism)

It’s a loss of calcium in the bones, goes to blood stream, excreted by kidneys, lands in organs through blood. 

Test: Pth, PTHrp; aldosterone level, glucorticoids?

Steroids and furosemide help body not absorb calc. Helps kidneys excrete calc into urine. 

*Test urine for calcium? Would be high if more is excreted into urine?

Fiber-gastro response food helps to fight calcium buildup, and renal CD diet. 

Addisons: auto immune disorder, with low corticoids, with inappetence, weight loss, lethargy, dehydration; also shock, low blood pressure. Poses like IBD and CKD. 

-does she have abnormally small adrenal glands?

-needs mineralcorticoids and steroids.

Cushings: hyperadrenocorticism, with increased thirst and urination, poses as CKD, muscle wasting, enlarged liver BUT increased appetite. Similar signs to diabetes.

Hyperaldosteronism: adrenal disorder. Caused by tumor in adrenal gland. Also idiopathic. Causes CKD. Or is misdiagnosed as CKD. With muscle weakness, lethargy, HIGH BLOOD PRESSURE (as with CKD, heart disease), loss of appetite.

-test with test to MSU.

High anioin gap-is metabolic acidosis. This test is an indicator of your pet’s acid:base balance, its blood pH and its bicarbonate buffer blood reserves. It is critical that the acidity (pH) of your dog or cat’s body be kept within a very tight range by the continual presence of carbonate (=bicarbonate=HCO3-) in its blood and your pet’s kidney’s ability to discharge excess chloride into its urine while conserving bicarbonate.

-caused by CKD, diabetes, When your pet’s blood sugar levels are not under control, the end result is metabolic acidosis – in this case lactic acidosis and ketoacidosis – as those products build up in your pet’s blood stream. A similar effect occurs in starvation, a cause of ketoacidosis as well. Also, lack of blood flow and oxygen to the body-heart disease, etc. Also-kidney, urine stones, blockages, A deficiency in aldosterone, as occurs in Addison’s disease can also cause a mild increased in your pet’s anion gap.

Ketoacidosis is a metabolic state caused by uncontrolled production of ketone bodies that cause a metabolic acidosis. While ketosis refers to any elevation of blood ketones, ketoacidosis is a specific pathologic condition that results in changes in blood pH and requires medical attention. The most common cause of ketoacidosis is diabetic ketoacidosis but can also be caused by alcohol, medications, toxins, and rarely, starvation.

High ALP- The main use of ALP is as a sensitive indicator of cholestasis in the dog (it will increase before bilirubin), however it is non-specific because corticosteroids (exogenous or endogenous “stress”) induces production of this enzyme, with subsequent increases in serum or plasma activity. In the cat however, ALP is a specific indicator of liver disease, whereas in large animals, the enzyme is less useful as it is insensitive, cholestatic disorders are infrequent, and reference intervals are quite broad.

The major isoforms that can be measured in animals are liver-ALP (L-ALP), corticosteroid-ALP (C-ALP; only in dogs), bone-ALP (B-ALP) and intestinal-ALP (I-ALP), but there are others including leukocyte-ALP and placental-ALP.

• Although alkaline phosphatase is considered a “liver enzyme,” it is produced by other cells, too.

• Alkaline phosphatase levels can be affected by many things, including certain medications and a variety of illnesses.

Certain medications, such as steroids, can cause this level to increase. Additionally, a variety of medical conditions can affect the ALKP level.

Most of the conditions that affect this enzyme cause the blood level to become elevated. The following are a few conditions that cause an elevated ALKP level:

• Pancreatitis (inflammation of the pancreas)

• Gall bladder disease

• Hepatitis (inflammation of the liver)

• Liver failure

• Cancer affecting the liver or bones

• Hyperadrenocorticism (Cushing’s disease)

• Diabetes

• Toxic injury to the liver

High albumin- Albumin is a major protein in a cat’s body that originates in the liver. 

Diseases indicated by low levels of albumin are as follows:

• Chronic liver disease

• Inflammatory Bowel Disease

• Pancreatitis

• Pyothorax (an infection in a cat’s chest cavity)

Unlike low levels of albumin, high albumin in cats has been found to be much less of a cause for concern. This is because, while low levels of albumin indicate loss, high levels indicate overproduction.

The most common high albumin cause is dehydration in your cat or a diet that is abnormally high in protein. While both dehydration and improper nutrition are a cause for concern, both can be easily fixed, and neither indicates underlying disease on their own.

High calcium can drive down PTH-high calc tells body PTH isn’t needed unless there’s a disease of the parathyroid. 

- High calc binds to phos, lowering phos.

-Magnesium acts as a phos binder if given more than body needs-good if need to drive down phos. 

*She has low phos-anemia? 

-low phos means low bicarb, danger to kidneys/indicates CKD

- high glucose levels might also be interfering with this phosphorous levels. Poorly controlled blood sugar levels or diabetes, might not allow the body to absorb phosphorous. 

-low phos indicates diabetes and hepatic acidosis; can be due to not eating well, too much calc or magnesium.

Katharine Has Multiple Organ Issues

Katharine is currently in the ER as I write. (1/28/24). She has developed CKD, liver disease, pancreatitis, and IBD, and of course heart disease. IBD/pancreatitis has been chronic for the last few years and worsened this fall. Liver disease is more recent although one value has been high for the past year. CKD was first thought to be a result of heart disease but has suddenly worsened with the onset of severe liver/IBD/Pancreatitis. In the ER she has low temperature, low heart rate, low glucose, and high liver and kidney values. She may need to be transferred to the vet hospital if she cannot be stabilized to come home.  She had a major seizure yesterday afternoon-not grand mal as everyone thinks is normal. Her seizures have never been more than her spacing out and falling over, unable to walk. When she had break out spaciness in 2021, additional phenobarbital always corrected them. Then she had a larger one and didn't respond to more phenobarbital, so an ER visit with oxygen and fluids was required. We increased her phenobarbital afterwards and she has been seizure free for two and a half years. Yesterday, she seemed fine. She ate, walked, was vocal, etc. But as she drank from the water bowl, she began to space out for a few minutes (from video footage.) I was in the other room when I heard a noise. When I found her, she was on the floor struggling to get up and water was everywhere. I gave her extra phenobarbital twice and she did not respond and began open mouth, fast breathing which she had never done before. I took her to the ER and they put her on oxygen, ran tests. All we know so far, is what I described. 

I was thinking back to Myrna Loy, our first cat with HCM, and for whom this blog and Facebook page were created. As much as I struggled to take care of her for 6 years and 9 months, I now look back and see that it was EASY compared to the cat issues I have dealt with in the last few years-Baby and Bette and now Katharine-because she responded to everything I tried. The only thing that never worked was rutin for the accumulation of lymphatic fluid called chylothorax.  She was so sick those last few months, and I was concentrating on fighting those issues that I did not try many rutin options. But still, she had CKD but it was mild until the very end but never in failure even as she died-two days before her values were good. 

But Baby and Bette and now Katharine-it's been a juggling nightmare with competing issues. For Katharine we respond to what we see in test results and exams and at home: is she eating, not eating? We need to hand feed her how much? What can she eat that the liver and pancreas will tolerate? She needs some fat for her body and medicines and vitamins; but she needs little fat for the liver and pancreas. Which appetite stimulant works and which one upsets the pancreas and liver?  Does she have IBD and needs an antibiotic? She needs to watch her sugar for the pancreas (it's not as if she eats sweets) and watch her sodium for her heart and watch her calcium because it is creeping up, and take a potassium supplementation in a pill and Renal K powder and Renal K gel so that it is normal instead of below normal because her kidneys and heart need a good strong level. She drinks a lot-so her urine appears dilute; but her specific gravity is low and her SDMA is high indicating declining kidney function. Myrna's urine was dilute from taking high levels of diuretics and we worked hard to keep her hydrated with water by mouth and in food, and with meds and making sure she drank enough. But her SDMA was normal until the end, and her specific gravity was normal until the end. Katharine has tremors and shakiness-neurological, pharmaceutical, disease related? 

And of course she seemed normal on Saturday before the seizure. She had eaten, been vocal, was moving around. I thought she had spent the week improving and was more stable. She had been eating more and we had been hand feeding less. She was mobile more. Had been engaged in toys more. And was climbing cat trees again. But the seizure hit her hard. And they think it hit because the liver-which processes phenobarbital-is acting up and may not have processed the phenobarbital well. (They did begin an additional seizure medication topiramate. But it is contraindicated with liver and CKD and causes anemia so may not be well tolerated in the long term.) But other things are going on that are causing low body temperature and low glucose and higher kidney and liver values. 

But what exactly? And what would be the point of an MRI, CT, or biopsy-requiring anesthesia which she cannot tolerate due to heart disease, and may not tolerate due to her current health issues-to discover other causes if she is dying of a disease or cancer that cannot be cured or fought because she cannot undergo anesthesia for treatments, treatments which may not prolong her life, and face having anesthesia causing heart failure, which then leads to her death of heart failure. If she did not have heart disease, I would go forward with an MRI and biopsy if needed. I would fight. And I will fight. But our options are few. We had a plan. We had a schedule. It was working. She was stable. And then she wasn't. That is what is hard for me to fathom. We work with what we know but then the body actually has something lying beneath the surface that throws a wrench into our process and into her health.