- Hepatic lipidose in cats - here in a case study
- History & signalement
- Clinical examination
- Diagnosis
- Diagnosis: hepatic lipidosis
- Treatment & result
- Treatment at a glance
- discussion
- background
- Primary vs. secondary hepatic lipidosis
- Clinical appearance
- Diagnosis
- diagnosis
- Treatment
- forecast
- Most important knowledge
- FAQs to hepatic lipidose in a cat
- Summary hepatic lipidosis in cats
- Sources:
Hepatic lipidose in cats - here in a case study
History & signalement
Pumpkin, a 7-year-old, 2.7 kg weighing, neutered domestic cat, was introduced to the emergency clinic after hiding in her nursing home for a week. She had been accommodated there after she had been handed over to an animal shelter. The caregiver could not determine whether pumpkin had eaten or drank. The evening before the performance, the caregiver Pumpkin got out of her hiding place and offered her wet and dry food, but she showed no interest. There was no information about the prehistory before the delivery in the shelter.
Clinical examination
During the clinical examination, Pumpkin was calm, attentive, responsive and anxious. The results showed a body condition score (BCS) of 2/5, expansed pupils, tachycardia (heart rate 208 BPM), urine stains on the pelvic extremes, Ikteric skin and scleras as well as ectaria and sticky mucous membranes. The dehydration was estimated at around 6–7 % due to the extended skin area, the capillary filling time was less than 2 seconds, and there were no signs of an enophthalmic appearance.
Diagnosis
The complete blood count (CBC) and serum chemistry (Table 1) showed a mild, normocytic, normochrome, non-regenerative anemia, increased old and alpic values, hyperbilirubinemia and hyperglycemia. Proteins and electrolytes were in the normal range. The coagulation examination and urine analysis showed no abnormalities, the primeval density was 1,041.
Table 1: Selected values from CBC & serum chemistry
| parameter | Result | Reference area |
|---|---|---|
| Hematocrit | 28 % | 30 %-45 % |
| Old | 395 u/l | 45-217 U/L |
| Alpine | 935 u/l | 11-95 u/l |
| Bilirubin | 7.2 mg/dl | 0-0.4 mg/dl |
| Glucose | 146 mg/dl | 60-133 mg/dl |
Abdominal sonography showed an enlarged liver with rounded caudoventral edges. The hepatic parenchyma appeared hyperechogenic and hyperate duking, which indicated a fat deposit. A fine needle aspiration of the liver showed numerous hepatocytes with pronounced vacuolization, which was compatible with lipid storage (Figures 1 and 2).
Figure 1
Fine needle aspirate from the liver of a cat. You can see a coherent leaf of numerous hepatocytes (pulled arrows). The cytoplasm of almost all hepatocytes is strongly stunned by large (macroesicular) and small (microvesicular) clear vacuoles, which often hide the cell nucleus and make it difficult to assess the hepatocytes. Numerous free lipid droplets can be seen in the background (dashed arrows). Modified Wright coloring, 200 times enlargement.
Figure 2
Fine needle aspirate from the liver of a cat. A coherent sheet of hepatocytes (pulled arrows) is visible. The cytoplasm is strongly bloated with clear vacuoles. Dark pigmented material (base casts; circles) between the cells indicates cholestasis. Numerous free lipid droplets (dashed arrow) are also available, but this finding alone is not diagnostic because lipids have to be detected intracellularly. Modified Wright coloring, 600 times enlargement.
No underlying disease was determined, so that a primary hepatic lipidosis, triggered by the stress of re -accommodation, was assumed.
Diagnosis: hepatic lipidosis
Treatment & result
Immediate inpatient admission with intensive therapy was recommended, but was rejected for financial reasons. Instead, a liquid bolus (0.9 % sodium chloride, 100 ml SC), vitamin K1 (1 mg/kg SC) and maropitant (1 mg/kg SC) were administered. Pumpkin was dismissed with the instructions to accommodate them in a closed area (e.g. large cage, bathroom) to prevent hiding at night. It should get water, but no food, and return the next morning to place an esophagostomy probe (E-probe).
To place the e-probe, Pumpkin was awarded with Butorphanol (0.3 mg/kg im), initiated with Propofol (4 mg/kg IV) and kept in oxygen with isofluran (1.5–2 %). The cat was positioned in a right side position, the left neck area was aseptically prepared, and the e-probe was placed. The probe was fixed with finger-trap stitching, closed and the neck area was supplied in terms of association in order to ensure access to monitoring. The recovery from anesthesia was without complications.
Energy requirement & feeding plan
The resting energy requirement (rer) was calculated as follows and was 183 kcal/day.
Rer kcal/day = 70 × (optimal body weight in kg)^0.75
A commercial, therapeutic critical-care diet, mixed with water at room temperature to a 1 kcal/ml porridge, was administered every 6 hours over 20 to 30 minutes in the first 3 days, from day 4 every 8 hours. The probe was flushed in front of (5 ml) and (10 ml) of any feeding with water. On the first day of treatment, 10 % of the RER were administered, spread over 4 meals (i.e. 18.3 ml of the Breis). In the following 9 days, the ration was increased by 10 % daily until the complete rer was reached. This frequency was retained until Pumpkin freely eaten. The details of the tailor -made feeding plan are shown in Table 2.
Table 2: Tailor -made feeding plan
| day | % of the rer (183 kcal/day) | Entire daily amount (ml) | Feeding frequency | Volume per feeding (ml) |
|---|---|---|---|---|
| 1 | 10 % | 18,3 | Every 6 hours | 4,57 |
| 2 | 20 % | 36,6 | Every 6 hours | 9,15 |
| 3 | 30 % | 54,9 | Every 6 hours | 13,7 |
| 4 | 40 % | 73,2 | Every 8 hours | 24,4 |
| 5 | 50 % | 91,5 | Every 8 hours | 30,5 |
| 6 | 60 % | 109,8 | Every 8 hours | 36,6 |
| 7 | 70 % | 128,1 | Every 8 hours | 42,7 |
| 8 | 80 % | 146,4 | Every 8 hours | 48,8 |
| 9 | 90 % | 164,7 | Every 8 hours | 54,9 |
| 10+ | 100 % | 183 | Every 8 hours | 61 |
Food was offered before each feeding over the E probe.
Lactulose (0.5 ml orally every 6 hours for 3 days, then every 8 hours) was administered to prevent clinical signs of hepatic encephalopathy. After about 2 to 3 weeks, Pumpkin showed interest in food. The amount recorded was deducted from the probe. After another 2 to 3 weeks, she was able to record all of her RER. Lactulose was discontinued and the E probe removed after eating for 4 days in a row.
Three weeks after the removal of the E probe, Pumpkin was adopted by her caregiver and described as healthy after three months when checking.
Treatment at a glance
- Polyionic fluid therapy without lactate or dextrose is recommended.
- Electrolytes should be monitored and disorders corrected .²
- Enteral nutrition is the key to treatment.¹⁻⁵
- Forced feeding is not recommended because it can lead to feeding or aspiration pneumonia.², ⁵
- Cats with a hepatic lipidose usually need a nasogastral (only stationary), esophageal or gastrostomal probe .² For home feeding, an e-probe is preferred.
- A breidiät with a high protein content, moderate fat content and minimal carbohydrates is crucial .³
- Feeding should be slowly started with small portions to avoid refeeding syndrome .³
- Appetititarians are not recommended .¹, ³
- Nutrition therapy can be lengthy and requires considerable commitment to the owner.³
- A relapse is rare for surviving cats.
discussion
The Feline Hepatic Lipidose (FHL) is the most frequently diagnosed hepatobiliary disease in cats. In the past, she was considered idiopathic, today it is known that it is caused by a negative energy balance.¹⁻⁵ The pathogenesis has not yet been fully clarified. FHL can affect cats of all breed, of all ages, with middle ages, overweight or formerly overweight cats and female animals.
background
Cats are mandatory carnivors and need a protein -rich diet with essential amino acids for their energy metabolism. A short phase of loss of appetite or hyporexia can lead to metabolic disorders.¹, ² With negative energy balance, lipase activity is stimulated in the peripheral adipose tissue in order to release fatty acids into the blood. These are absorbed by the liver, oxidized and either installed in VLDL (very-low-density-lipoproteins) or stored as a triglycerides intracellularly.¹ In anorectic cats, most triglycerides are stored due to the limited oxidative capacity and VLDL redistribution in Lebernervakuol.
The excessive accumulation of triglyzerides leads to enlargement of the hepatocytes, increased liver weight and to change the liver architecture, which results in cholestasis, Ikterus, reduced metabolic capacity and ultimately liver failure .¹⁻³ Cytological examinations show in more than 80 % of hepatocytes.
Primary vs. secondary hepatic lipidosis
FHL can occur primarily or secondary. Primary FHL arises when external factors such as unpalatiled feed, environmental stress or food uncertainty lead to insufficient calorie intake. The secondary FHL accounts for 95 % of cases and develops as part of another, progressive disease (e.g. neoplasia, diabetes mellitus, inflammation or kidney disease) that leads to anorexia
Clinical appearance
The clinical symptoms include dehydration, nausea, hypersalivation, vomiting, Ikterus, Stumpfesk, lack of fur care, constipation, diarrhea and a history of loss of appetite or weight loss. Cats with FHL are often hyperglycemic due to insulin resistance and increased production of counter -regulatory hormones. ² Hypoglycemia is a sign of a serious illness in these cases and indicates liver failure in the final stage.
Diagnosis
Parameters of the blood count are often inconspicuous. Unspecific findings such as mild, non -regenerative anemia or leukocytosis can occur, but often depend on the underlying cause. A thrombocytopenia is not expected in primary FHL, unless there is a disseminated intravascular coagulation before²
Bleeding is common in cats with FHL, especially during IV catheter placement, blood sample, liver biopsy or probe placement .² vitamin K-dependent coagulation factors (II, VII, IX, X) are produced in the liver as non-functional precursors that require vitamin K for activation. Since vitamin K is fat -soluble and the memory in the body is limited, regular absorption through food is necessary. Hepatobile diseases can lead to a secondary vitamin K deficiency due to inadequate fat digestion and absorption. In a study, 75 % of cats with FHL showed increased pivka values (proteins induced by vitamin K deficiency), ¹ which indicates a widespread vitamin K deficiency in FHL. Therefore, the Protrombin time and the activated partial thromboplastin period in FHL patients are often extended .²
diagnosis
The suspicion diagnosis is often based on anamnesis, clinical examination, laboratory values and imaging .² The final diagnosis is usually made by cytological examination of a fine needle aspirate. This technology can usually be carried out without general anesthesia and has a lower risk of bleeding than a larger biopsy. However, if the fine needle aspirate does not provide a diagnosis, a larger biopsy may be required .²
Treatment
Treatment is uncomplicated, but an early start of therapy and close monitoring significantly improve the forecast. Serum chemistry, urine analysis, CBC and coagulation profiles should be carried out in all suspected cases in order to steer the therapy, to determine the severity and to recognize possible causes .², ⁵
If FHL is suspected, prophylactically vitamin K1 (0.5–1.5 mg/kg in or SC) should be administered in order to reduce the risk of bleeding during interventions. Liquids without lactate or dextrose are preferred because they can negatively influence the hepatic fat metabolism.¹ As soon as the hydration status and the electrolyte are stabilized, a high -quality diet with a high protein content (33–45 %), moderate fat content and low carbohydrate content should be administered, preferably via a nasal probe (only stationary), esophagiostomy (preferably for home) or gastrostomy to ensure sufficient calorie intake.
A feed structure that is too fast can lead to refeeding syndrome and cause severe, life-threatening electrolytic disorders. An initial permanent infusion in small quantities can be helpful .³ Appetititis is not recommended due to unpredictable results, changed liver metabolism activity and masking effects.¹, ³
Feeding should begin with a maximum of 20 % of the calculated RER, divided into 4–5 small meals or as continuous infusion. Then the amount is increased by 10 % daily, while paying attention to signs of gagging or swallowing is observed .³ In the case of swallowing or swallowing, the amount of feed for the next 12 hours should be reduced by 50 %. Food should be heated to space to body temperature before each feeding. A water bath is preferable to the microwave to ensure even warming. Before feeding, the probe is rinsed with 5 ml of water to avoid constipation. After feeding, it is also washed up with approx. 10 ml of water.³
The authors recommend carrying out each feeding over at least 20 to 30 minutes. Since Pumpkin responded well to 6-hour feeding after a few days, the frequency for better compliance with the caregiver was reduced to every 8 hours.
A study on the effect of diacylglycerol-o-acyltransferase-1 inhibitors on the trigly cerver enrichment at FHL showed that the active ingredient T863 reduced the trigly cerver enrichment by 52 %.
forecast
Without treatment, the survival rate is only 5–20 %. With therapy, the survival rate increases to 50–60 % for secondary FHL and to impressive 80–88 % in primary FHL.²⁻⁴
The forecast largely depends on the presence of an underlying disease and the early start of enteral nutrition. Owners should be informed that the probe nutrition requires a high level of participation and can extend over 3–6 weeks .³ Relapses are rare for surviving cats .⁵
Most important knowledge
- FHL is an excessive triglycerid enrichment in the hepatocytes as a result of negative energy balance and the most common hepatobile disease of the cat.
- FHL is life -threatening and requires quick treatment.
- Middle-aged, overweight cats or those with obesity history are particularly at risk-but FHL can affect cats of all breed, of all ages or gender .¹, ²
- Early intervention is crucial for the success of the treatment.
- The chances of recovery are high, especially with primary FHL.
FAQs to hepatic lipidose in a cat
What is the most common cause of hepatic lipidosis in cats?
The most common cause of the development of hepatic lipidosis is a negative energy balance, i.e. if a cat absorbs too little energy in the form of food over a longer period of time. Cats that suddenly stop eating through external stress factors such as a move, a new environment, change of feed or illness suddenly stop. This so -called primary form of hepatic lipidosis occurs if no other underlying disease can be determined.
There is also the secondary form that makes up about 95 % of cases. This is a consequence of other diseases such as diabetes mellitus, chronic kidney diseases, inflammation of the digestive tract or tumor diseases. These underlying diseases often mean that the cat becomes faithful or stops eating, which subsequently leads to a massive release of fatty acids from the body fat into the liver.
No matter whether primary or secondary - it is crucial that the cat remains malnourished over a certain period of time. Since cats as mandatory carnivors rely very strongly on continuous energy supply, they can only get into the dangerous state of hepatic lipidosis after just a few days of refusal to eat.
How do I recognize the signs of a hepatic lipidose in my cat early on?
Early detection is crucial to significantly increase the chances of recovery. Typically, cats with the beginning hepatic lipidosis initially show unspecific symptoms, but they should be taken seriously. Above all, this includes an lack of appetite or completely refusal to eat over more than 24–48 hours. This should already be a warning signal, since cats are particularly sensitive to phases of food leave.
Other signs are weight loss, lethargy, weakness or reduced activity. Also an increasing yellow color (Ikterus) of the mucous membranes, the gums, the scleras (white white) or the skin indicates a participation of the liver. Often the fur becomes stump, the cat neglects the grooming, and vomiting or diarrhea can occur.
In later stages, the general condition deteriorates drastically: neurological symptoms such as disorientation or seizures occur due to possible hepatic encephalopathy. Anyone who recognizes these warning signs early and immediately visits veterinary help can significantly slow or even stop the progression of the disease.
How is the hepatic lipidosis diagnosed in cats?
The diagnosis of the hepatic lipidosis is based on a combination of anamnesis, clinical examination, laboratory examinations and imaging methods. Veterinarians pay particular attention to the history of loss of appetite or weight loss as well as clinical symptoms such as Ikterus or weakness.
In the laboratory picture there are often increased liver values (especially old and alp), hyperbilirubinemia, hyperglycaemia and sometimes signs of light anemia. The ultrasound examination also provides valuable information: an enlarged, hyperechogenic liver indicates an obesity.
For a final diagnosis, a fine needle aspiration of the liver is usually carried out. A small amount of liver tissue is removed with a thin needle and microscopically examined. Characteristic are numerous vacuoles filled with fat in the hepatocytes. This minimally invasive procedure is low -risk and usually quickly provides the crucial clarity.
In addition, special coagulation tests to control bleeding and the measurement of vitamin K-dependent factors can be carried out in addition, since many cats with FHL have a coagulation disorder.
What does the treatment of hepatic lipidosis look like and how long does it take?
The treatment of hepatic lipidosis in cats is intense, but with a good prognosis if it begins early. The focus is always on the controlled, gentle resumption of food intake. Since affected cats usually do not eat voluntarily, feeding via a nutritional probe (usually an esophagostomy probe) is often necessary.
First, the calm energy requirement (rer) of the cat is calculated, and the amount of food is slowly increased to avoid the dangerous refeeding syndrome. Usually you start with 10–20 % of the energy requirement and increase the amount by about 10 % daily until the full calorie intake is reached.
In parallel to nutritional therapy, supporting measures such as liquid therapy, vitamin K-gifts to support coagulation as well as medication against nausea or accompanying diseases are administered. In some cases, lactulosis is also used to minimize the risk of hepatic encephalopathy.
The entire duration of treatment varies greatly, but is usually several weeks - often between 3 and 6 weeks. Even after removal of the probe, the diet should be monitored exactly and the cat should be checked closely. Good news: If the cat survives the acute phase and absorbs food independently, the forecast is usually excellent, and relapses are rare.
Can I prevent a hepatic lipidosis of my cat?
Yes, there are quite effective measures to prevent hepatic lipidosis - especially if your cat belongs to a risk group, for example because it is overweight or suffers from a chronic illness. The most important prevention target is to ensure that your cat always eats regularly. A diet of 24–48 hours should already be taken seriously and veterinarian should be clarified.
Weight management plays a central role: overweight cats should be carefully brought to a healthy weight, but always under veterinary supervision. Diets that are too fast are dangerous and can trigger the lipidosis that you want to prevent.
Stress minimization is also an important factor. Changes such as moves, new family members (humans or animals) or conversions should be designed as gently as possible so that your cat does not set the eating out of fear or uncertainty. Especially with planned changes, it helps to maintain the usual food and offer any tasty additions.
Last but not least: regular health checks help to recognize potential diseases at an early stage that could be triggered as a trigger for secondary hepatic lipidosis. With attention, good care and timely action, the risk can be significantly reduced.
Summary hepatic lipidosis in cats
Hepatic lipidose in cats is one of the most common and serious liver diseases that cat owners should know. It is particularly tricky that the hepatic lipidosis in cats often begins with gradual symptoms and is therefore unfortunately often recognized too late. A sudden loss of appetite is one of the first alarm signals for the hepatic lipidosis in cats .
The cause of the hepatic lipidosis in cats is usually a negative energy balance in which fat reserves are broken down from the body and stored in the liver. This overload of the liver cells with fat is typical of the hepatic lipidosis in cats and can quickly become life -threatening without timely treatment. Overweight animals are particularly susceptible to hepatic lipidosis in cats , but normal -weighted cats can also be affected.
The symptoms of hepatic lipidosis in cats are diverse. They range from loss of appetite to weakness to jaundice. hepatic lipidosis show vomiting, lethargy or neurological failures in cats. The early detection of the hepatic lipidosis in cats is therefore crucial for the success of the treatment.
The diagnosis of hepatic lipidosis in cats includes blood tests, a sonography of the liver and a fine needle aspiration. The latter usually reliably confirms the presence of a hepatic lipidosis in cats by making the liver cells typical of this disease visible.
The therapy of hepatic lipidosis in cats is intense, but promising. The cat is slowly getting used to sufficient calorie intake via a nutritional probe. At the same time, the hepatic lipidosis in cats a supportive therapy with liquids, electrolytes and, if necessary, vitamin K. The careful feeding is the central element in the treatment of hepatic lipidosis in cats .
With patience and consistent care, many cats can completely survive hepatic lipidosis in cats Especially with early hepatic lipidosis in cats, the chances of recovery are 80 to 88 percent. Even with secondary hepatic lipidosis in cats , which is triggered by a underlying disease, the forecasts are good, even if the underlying disease is treated.
Prevention also plays a central role. Anyone who knows the risk factors for the hepatic lipidosis in cats can counteract early. This includes avoiding obesity, a stress -free environment and the immediate veterinary presentation in the event of appetite loss. hepatic lipidosis in cats can be significantly reduced.
Pet owners should know that the hepatic lipidosis in cats is not a death sentence. With timely diagnosis, intensive therapy and good care, there is a real chance of complete healing cats in cats
The close cooperation with the veterinarian team is essential to positively influence hepatic lipidosis in cats Patience and commitment pay off, because the hepatic lipidosis in cats requires weeks of care. But the effort is worth it: cats that survive the hepatic lipidosis in cats usually lead a normal life again.
In summary, it can be said that the hepatic lipidosis in cats is a serious but treatable disease. Attention in everyday life, quick reaction to first symptoms and well -founded medical care can prevent hepatic lipidosis from taking on a life -threatening extent in cats .
Knowing the hepatic lipidosis in cats helps cat owners to minimize risks and act quickly in an emergency. The diagnosis of hepatic lipidosis in cats not become fate, but an overwhelming challenge on the way to a healthy cat life.
Sources:
- Center SA. Feline Hepatic Lipidosis. Vet Clin North am Small Anim Pract . 2005; 35 (1): 225-269. DOI: 10.1016/J.CVSM.2004.10.002
- Valtolina C, Favier Rp. Feline Hepatic Lipidosis. Vet Clin North am Small Anim Pract . 2017; 47 (3): 683-702. DOI: 10.1016/J.CVSM.2016.11.014
- Armstrong PJ, Blanchard G. Hepatic Lipidosis in Cats. Vet Clin North am Small Anim Pract . 2009; 39 (3): 599-616. DOI: 10.1016/J.CVSM.2009.03.003
- Brown B, Mauldin GE, Armstrong J, Moroff SD, Mauldin Gn. Metabolic and hormonal alterations in cats with hepatic lipidosis. J VET intern . 2000; 14 (1): 20-26. Doi: 10.1892/0891-6640 (2000) 014 <0020: Mahaic> 2.3.co; 2
- Webb CB. Hepatic Lipidosis: Clinical Review Drawn from Collective Effort. J Feline Med Surg . 2018; 20 (3): 217-227. DOI: 10.1177/1098612x18758591
- Haaker MW, Kruitwagen HS, Vaandrager, et al. Identification of Potential Drugs for Treatment of Hepatic Lipidosis in Cats Using an in Vitro Feline Liver Organoid System. J VET intern . 2020; 34 (1): 132-138. Doi: 10.1111/JVIM.15670