Clinical and pathological staging, AJCC 2009
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More than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\\n\\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\\n\\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\\n\\nAdditionally, each book published by IntechOpen contains original content and research findings.
\\n\\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\\n\\n\\n\\n
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'
Simba Information has released its Open Access Book Publishing 2020 - 2024 report and has again identified IntechOpen as the world’s largest Open Access book publisher by title count.
\n\nSimba Information is a leading provider for market intelligence and forecasts in the media and publishing industry. The report, published every year, provides an overview and financial outlook for the global professional e-book publishing market.
\n\nIntechOpen, De Gruyter, and Frontiers are the largest OA book publishers by title count, with IntechOpen coming in at first place with 5,101 OA books published, a good 1,782 titles ahead of the nearest competitor.
\n\nSince the first Open Access Book Publishing report published in 2016, IntechOpen has held the top stop each year.
\n\n\n\nMore than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\n\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\n\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\n\nAdditionally, each book published by IntechOpen contains original content and research findings.
\n\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\n\n\n\n
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In this chapter, cutaneous metastases from malignant melanoma will be analyzed from a clinical and a prognostic point of view.
This non rare condition is often distressing for the patient, as cutaneous lesions increase progressively in number and size and are frequently worsened by ulceration, bleeding and pain.
After a general introduction about the incidence of cutaneous involvement in melanoma natural history, clinical classification of skin metastases will be provided. Then, the impact of cutaneous localizations on prognosis will be evaluated. In the last paragraph, the different therapeutic options for the management of patients with loco-regional or diffused cutaneous metastases will be reviewed.
Skin metastases from solid tumor are not rare. They affect an estimated percentage of patients ranging from 0.7 to 9% in several literature series (Spencer & Helm 1987, Lookingbill, Spangler & Helm 1993, Schwartz 1995, Hu et al. 2008), in the late phases of disease progression or, in more than 7% of patients, as first sign of disseminated disease (Lookingbill, Spangler & Helm 1993, Rosen 1980). Breast cancer is the most commonly involved tumor, accounting for more than 60% of cases of cutaneous spread, followed by colon carcinoma (Krathen, Orengo & Rosen 2003). Moreover, cutaneous metastatic disease is commonly seen with cancer of the lung, kidney and ovary and with sarcoma, lymphoma or leukemia.
As expected, tumor types are differently distributed among the two genders: lung, colon and head and neck tumours together with melanoma account for the majority of skin metastases in males; whereas, breast cancer is the most common neoplasm related to the development of cutaneous secondary lesions in females (Hu et al 2008).
Focusing on melanoma, skin metastases represent a relatively frequent event in the natural history of the disease and can develop in early as well as in late stage of disease. Cutaneous or subcutaneous lesions arise in 10-17% of patients affected by melanoma and almost the 50% of patients with metastatic disease develops skin involvement (Lookingbill, Spangler & Helm 1993, Schwartz 1995, Krathen, Orengo & Rosen 2003).
No specific clinical or histological characteristics were found in patients with cutaneous metastases from melanoma if compared to those with visceral localizations (Savoia et al 2009). However, known risk factors related to prognosis impact on the metastatic melanoma potential.
On the basis of the distance from the primary melanoma, skin metastases are described as local recurrences, in transit disease or distant metastases.
True local recurrences are defined as the reappearance of melanoma in -or contiguous with- an excision scar or a graft and bearing an in situ component (Olsen et al 1970; Brown & Zitelli 1995). The prognosis of local recurrence defined strictly in this way is much better than that associated with in transit disease and 5-year survival rate is related only to the thickness of the primary melanoma. These recurrences are in fact considered as a result of a uncompleted resection of primary melanoma, and are for this reason becoming rare.
In-transit disease (satellitosis) indicates cutaneous or subcutaneous disease between the primary site and the regional lymph nodes. Satellite nodules and in-transit disease are associated with worse prognosis (super imposable to a melanoma with nodal metastases; stage III disease), and the distance of cutaneous deposits from the primary site has no prognostic significance (Balch et al 2009).
Distant cutaneous metastases are defined as tumour lesions that grow in any skin site over the regional lymph nodes. The presence of any distant metastases delineates a stage IV disease, even if patients with sole distant skin metastases (and normal serum LDH levels) have a relatively better prognosis if compared with those of other metastatic patients (Balch et al 2009). Obviously, distant skin melanoma localization can appear together with or in absence of other visceral metastases. Stage and prognosis vary according to AJCC classification as shown in table 1 (Balch et al 2009).
Clinical Staging | Pathological Staging | ||||||
0 | Tis | N0 | M0 | 0 | Tis | N0 | M0 |
IA | T1a | N0 | M0 | IA | T1a | N0 | M0 |
IB | T1b | N0 | M0 | IB | T1b | N0 | M0 |
T2a | N0 | M0 | T2a | N0 | M0 | ||
IIA | T2b | N0 | M0 | IIA | T2b | N0 | M0 |
T3a | N0 | M0 | T3a | N0 | M0 | ||
IIB | T3b | N0 | M0 | IIB | T3b | N0 | M0 |
T4a | N0 | M0 | T4a | N0 | M0 | ||
IIC | T4b | N0 | M0 | IIC | T4b | N0 | M0 |
III | any T | N 1-3 | M0 | IIIA | T1-T4a | N1a/2a | M0 |
IIIB | T1-T4b | N1a/2a | M0 | ||||
T1-T4a | N1b/2b | M0 | |||||
T1-T4a/b | N2c | M0 | |||||
IIIC | T1-T4b | N1b/2b/2c | M0 | ||||
any T | N3 | M0 | |||||
IV | any T | any N | M 1 | IV | any T | any N | M 1 |
Clinical and pathological staging, AJCC 2009
Skin metastases from melanoma can arise as single or multiple nodules. The most common presentations of cutaneous metastatic disease are brown to black or skin colored papules and nodules, sometimes ulcerated. In the majority of these cases cutaneous metastases were correctly identified by the clinician before the pathologic diagnosis was given; dermoscopy could help in diagnosis, even if skin melanoma metastases have often aspects that are indistinguishable from the characteristic pattern of blue nevi (Carlos-Ortega, de Oca-Monroy & Isyta-Morales 2008). Epidermotropic melanoma metastases are histopatologically characterized by aggregates of atypical melanocytes within the dermis with thinning of the epidermis. Usually there is no lateral extension of atypical melanocytes within the epidermis beyond the concentration of the metastases on the dermis. Metastases differs from primary melanoma by the absence of inflammatory infiltrate and junctional activity, even if a prominent lymphocytic infiltrated can be sometimes observed. In few cases metastatic cells are small and nevoid, with few or any mitoses and differentiation from compound nevi is difficult (Elder E et al, 2005. Tumours and Cysts in dermis and Subcutis, in: Lever’s histopathology of the skin. Lippincott Williams&Wilkins, Philadelphia).
Less frequently, a wide morphological spectrum of lesions has been described, including erythematous patches or plaques, inflammatory erysipela-like lesions, diffuse sclerodermiform lesions with indurations of the skin (‘‘en cuirasse’’ metastatic carcinoma), telangiectatic papulovesicles, purpuric plaques mimicking vasculitis, and alopecia aerate-like scalp lesions (Saeed, Keehn & Morgan 2004, Sariya et al 2007). In these cases, clinical diagnosis could be more challenging and metastases can be suspicious for benign entities (Figure 1).
Clinical features of local recurrences that are defined as the reappearance of melanoma in or contiguous with an excision scar or graft and bearing an in situ component.
Moreover, there are also rare cases of so-called zosteriform metastases, with vesicobullous herpetiform lesions or papules and nodules distributed along one or more dermatomes. A previous Varicella Zoster Virus (VZV) infection or widespread lymphatic obstruction by tumor cells can justify the zosteriform pattern (Figure 2).
Zosteriform metastases among thoracic dermatomes.
However, zosteriform metastases, as well as the rare skin metastases occurring on skin graft donor site, could be explained as a Koebner phenomenon (Savoia et al 2009, Marenco et al 2009).
From a clinical point of view, if bleeding and super-infection are not present, superficial skin metastases are usually asymptomatic, even if patients frequently report localized pain and paresthesiae anticipating the onset of clinically evident cutaneous lesions; these symptoms are related to oedema and mechanical stress on the near tissues and usually disappear in a few days. On the other hand, when subcutaneous lesions grow deep infiltrating muscles or nerves become very painful. The management of pain in these cases could be difficult and requires a multidisciplinary approach.
As mentioned earlier, bleeding and super-infections are the most frequent complications of skin metastases and can significantly impact on the patient\'s quality of life (Kaheler, Egeberts & Hauschild 2010). These complications can also compromise general conditions. Massive bleeding from cutaneous metastases could become life threatening; sepsis related to the bacterial dissemination of infected metastases represents an uncommon but not rare event, that lead to septic shock and death (Figure 3).
Infected diffuse metastases from malignant melanoma
Cutaneous secondary lesions can occur on all anatomic sites, with skin metastases from other solid tumours more frequently found on the head, neck, anterior chest and abdomen, whereas lower extremities are rarely involved (Schwartz, 1995). Conversely, skin metastases from melanoma are more frequently observed on the back in men and on the lower limbs in women. These different patterns of cutaneous localizations among sex can be explained by the fact that in more than 30% of cases, secondary cutaneous localizations occur in the same anatomic area of the primary (Savoia et al 2009).
In more than half of the cases, skin represents the first site of metastatic involvement after the primary melanoma diagnosis. In about one third of cases, patients develop skin involvement after evidences of regional lymph nodal metastatic disease.
The finding of concomitant distant cutaneous, visceral and nodal metastases account for more than 10% of cases, whereas skin involvement after visceral dissemination is rare, and occurs only in about the 3% of patients (Savoia et al 2009).
Cutaneous metastases are loco regional in nearly 80% of cases, whereas distant metastases were documented in the remaining 20% of patients. A different pattern of cutaneous metastases was related to the time of onset: when cutaneous metastases arise as the first site of relapse, there is a significant higher percentage of locoregional localizations, whereas distant skin involvement was more frequently observed after visceral involvement. No significant differences were found between patients with regional and those with distant metastases regarding to the known risk factors, such as Breslow thickness, Clark level, histotype of the primary melanoma and ulceration (Savoia et al 2009).
It is noteworthy that in patients with distant metastases, primary melanomas arose predominantly at trunk and back, whereas patients with cutaneous loco-regional spreading were affected mainly by primary located at leg and foot. As we know, loco-regional metastases develop as a result of tumour cell embolization in the dermal lymphatic vessels between the primary tumour site and the draining regional lymph node basin; lymphatic stasis to lower limbs consequent to nodal dissection represents an additional risk factor for cutaneous locoregional dissemination.
In contrast, the correlation between disseminated skin lesions and primary melanoma located to the trunk could be explained by the fact that the lymph drainage of this region is not strictly dependent on a single station, but it could be resulted from more than one lymphatic basin, together with a possible role of haematogenous spreading.
Disease free survival evaluated from the first melanoma diagnosis varies in relation to the first site of metastatization. In our experience, loco regional cutaneous relapses develop early, but show a very late progression to visceral disease. On the contrary, patients with disseminated skin lesions as first site of relapse had a longer disease free interval from the first diagnosis but a shorter time to progression to visceral metastases (Savoia et al 2009).
The choice of the modality of treatment for cutaneous melanoma metastases depends on several factors, including location and number of lesions, presence of systemic involvement, age and general health conditions of patients. Moreover, the prognostic differences between patients with loco-regional and distant skin metastases justify different approaches in their clinical management.
Important therapeutic options including surgery, isolated limb perfusion, local or systemic chemo- and immuno-therapy and radiotherapy are discussed in detail below.
Surgery is the gold standard and represents the most effective treatment for limited in-transit disease, when technically feasible. It is an adequate treatment when the lesions are relatively small and clustered in a reasonable circumscribed area. Primary melanoma should be excised widely with a 1-2 cm margin depending on Breslow thickness, whereas wide surgical margins are unnecessary for the treatment of cutaneous metastases. Usually, metastases are clearly demarcated from the surrounding normal dermis and overlying epidermis and the better approach is the complete macroscopical excision of the lesion. When microscopical involvement of margins is documented, reintervention is not mandatory (Hoekstra, 2008).
If technically possible, direct wound closure is to prefer; the second choice is represented by skin graft, because plastic surgical reconstruction can affect the lymphatic drainage pattern.
Palliative treatment should be considered when results in the control of local complications (e.g. bleeding) and/or in a consistent quality of life improvement.
Amputation should be only considered as palliation for imminent exsanguinating haemorrhage or fungation unacceptable for the patient.
Isolated limb perfusion (ILP) -firstly described by Creech and Krementz in 1958- can deliver high doses of cytotoxic agents to a limb, minimizing systemic toxicity. The dose received regionally can be up to tenfold higher than the systemic mean tolerated dose. Isolated limb perfusion is widely indicated for patients with advanced or recurrent in-transit disease, showing a complete response rate around the 50% in the majority of the published series, with an overall response rate up to 80% (Lens & Dawes 2003, Rossi et al 2010). On the contrary, the role of isolated limb perfusion as adjuvant therapy is still debated (Hoeckstra 2008). The tumour response after perfusion is the only demonstrated prognostic factor affecting local control of the disease and overall survival (Rossi et al 2010).
The usual agent employed is melphalan, with or without tumour necrosis factor (TNF); TNF increases response rate thanks to its selective disruption of the tumour microvasculate, with a consequent ischemic damage of melanoma cells, even if seems not to influence the long term local control (Di Filippo et al 2006). Dacarbazine is less effective when administered regionally; other combinations of cytostatics (dactinomycin, nitrogen mustard, vindesine, thio-TEPA) have also been proposed but the published series are too small to give absolute conclusions (Daryanani et al 2000, de Wilt et al 2000, Hoeckstra 2008). Hyperthermia, with temperature between 39 to 41 act sinergically with high dose chemotherapy, even if can exacerbate loco regional toxicity (Hoeckstra 2008).
General anesthesia is required. However, age does not represent a contraindication to ILP. Systemic side effects, due to drug releasing into the systemic circulation are rare and mainly represented by nausea, vomiting and mild bone marrow suppression. Local toxic reactions are more frequently described and ranges from mild erythema to deep tissue inflammation; nearly 25% of patients develop neuropathy or pain, whereas chronic edema is usually related to lymphoadenenctomy (Bonifati et al 2000, Rossi et al 2002).
Recently, electrochemotherapy (ECT) has been proposed as a new treatment modality for skin metastases of different malignancy, including melanoma. ECT enhances membrane permeability by electric pulses thus permitting a major drug delivery in neoplastic cells and a better cytotoxic effect.
Bleomycin and cisplatin are the drugs more frequently used in ECT with an increased efficacy up to 8.000-fold for bleomicyn, and up to 80-fold for cisplatin (Gaudy et al 2006).
The ECT technique requires only a regional anesthesia or mild general sedation with a lower duration if compared to isolated limb perfusion. With respect to ILP, ECT shows a minimal systemic toxicity; treatment is generally well tolerated; side effects were mainly represented by erythema and edema at the site of treated lesions, superficial erosions, scars and permanent marks from the electrodes (Quaglino et al 2008). Thus ECT can be performed also in patients with major co morbidities.
The first large study about effectiveness of ECT in melanoma treatment, was the multi center European Standard Operating Procedure of Eettrochemoterapy (ESOPE), based on the new CliniporatorTM Elettric Pulse Generator; this study enrolled twenty melanoma patients, with an overall response rate of more than 20% (Marty et al 2008). Several papers recently published confirm these encouraging results of ECT in the control of skin metastases (Campana et al 2009, Moller et al 2009). In our experience, the global response rate was of 79.4, with a percentage of complete remissions of 23.2%(Quaglino et al 2008); complete response was defined in accordance World Health Organiziation (WHO) guidelines as the total clinical disappearance of the tumor (WHO. From Handbook for Reporting Results of Cancer Treatment, vol 48; pp 22-27. Geneva, 1997).
The lesion size was the most predictive parameter for response; response rate for larger lesions was significantly lower. Moreover, a second limit is represented by the possible relapse of new lesions on untreated areas: ECT represent in fact a local treatment. However, it is possible to repeat ECT, both on new metastases in untreated areas and on already treated lesions with a previous partial remission or no changes. In our experience, new responses were obtained in about 60% of retreated lesions.
Appropriate dressing should be performed with the aim to control ulceration of cutaneous tumours, local infectious complications and to ensure an acceptable quality of life.
The effectiveness of radiotherapy in the treatment of melanoma metastases is still debated. A poor response was historically observed on in vitro cultures from melanoma cells treated with external-beam radiation (Barranco, Romsdahl & Humphrey 1971). So, radiotherapy was mainly used as palliation when disease was too extensive for surgery and other modalities of treatment were inadvisable or ineffective in stage III and IV melanoma patients. However, a retrospective review (Fenig et al 2009) showed a 52% response rate in stage IV patients who received radiotherapy with palliative intent and others studies (Sause et al 1991; Seegenschmeid et al 1999) demonstrated an overall response rate ranging from 60 to 79% for stage III disease. Moreover, disease-free and overall survival seems to be significant longer in patients who received radiotherapy (Olivier et al, 2007).
Usually, chemotherapy plays a role in the treatment of stage IV melanoma patients with visceral metastases. Regarding cutaneous metastases, chemotherapy can be used in patients with wide spread skin lesions not eligible for local treatments, with or without a concomitant visceral involvement.
Chemotherapy could be used also in stage III, when other loco-regional treatments have failed or are technically not feasable (e.g. cutaneous lesions diffused at trunk or back).
The global response rate is less than 25% for single agent treatment. The gold standard is still represented by Dacarbazine; new molecules as Temozolomide and Fotemustine showed a super imposable disease-free and overall survival, with major toxicity (Middelton et al, 2000). Combination regimens or chemo-immunotherapy give higher response rate but also more severe side effects. However, response to chemo-immunoterapy is not related to statistically significant benefit in term of overall survival when compared with a single-agent treatment.
Recently, Ipilimumab, a human anti-CTLA4 monoclonal antibody showed objective responses or disease stabilization in patients with advanced melanoma (O\'Day et al, 2010). No data about the effectiveness of Ipilimumab in the treatment of cutaneous metastases are available, even if several studies are ongoing.
The response rate for in transit metastases treated with dacarbazine is 15-20%; the majority of the responses are partial with a median response duration less than 6 months. Chemoimunotherapy showed also no survival benefit (Hoekstra 2008).
Finally, the clinical efficacy of RAF inhibitors in BRAF mutated melanoma patients are under evaluation after some encouraging preliminary report; a phase I study on patients with both disseminated cutaneous and visceral metastases reported an 81% of clinical responses in patients treated with selective BRAF inhibitor, with a median time to progression of 6-9 months (Flaherty, 2010).
Patients with small (<2 cm) and superficial lesions who are not suitable for isolated limb perfusion, ECT or other conventional modalities of treatment can be considered for carbon dioxide (CO2) laser ablation. This therapy is minimally invasive: only local anesthesia is required and the resultant defect does not require surgical closure but can be covered with a dressing until secondary healing (Lingam & McKay, 1996; Gibson, Byrne & Mc Kay, 2004). So, can be considered a minimally invasive and effective method of palliation; the role as first line treatment is still debated, in fact the technique can be used to treat only visible and superficial lesions, while deep subcutaneous metastases, large volume lesions and microscopic disease can not be treated with laser ablation (Gimbel, Delman & Zager, 2008).
This technique uses temperatures from -50 C to -60 C (with nitrogen spray) to obtain direct tissue destruction. The heat transfer results in vascular stasis, ice crystal and disruption of cell membranes, Ph changes, hypertonic damage and thermal shock that lead to tissue damage and necrosis. Low temperature causes the development of a bulla and a secondary healing with a scar. After the introduction of laser ablation and ECT, cryosurgery is less frequently used in the treatment of cutaneous metastases from melanoma (Hoekstra, 2008).
The intralesional injection of bacillus Calmette-Guérin (BCG) was the first immunotherapy used in the local treatment of cutaneous metastases from melanoma. This procedure was accompanied by sever complications such as ulceration, skin necrosis, and superinfection without significative improvement of lesions treated (Tan & Ho, 1993). Other drugs such as IL-2, INF alpha and dinitrochlorobenzene, with or without sistemic dacarbazine, were more recently used as intralesional therapy (Radny et al, 2003; Strobbe et al, 1997); results are still debating and further investigations are necessary. Encouraging results regarding high-dose intratumoral IL-2 administration in melanoma patients with cutaneous secondarities has been reported (Weide et al, 2010): a complete local response was described in more than 60% of melanoma patients and seemed to be associated with an increased responses to subsequent chemotherapies. Recently, phase I studies confirmed the safety and an enhanced immune response for intralesional injection of Allovectin in metastatic melanoma patients. Unfortunately, phase II studies showed a complete response in only the 3.1% of treated patients, with an overall response rate of 11.8% and a median time-to-progression of 1.6 months (Beidikan et al, 2010).
Rose bengal has been proposed as a possible intralesional treatment, with an objective response rate ranging from 27 to 69%, related to the dose of injection (Thompson, Hersey & Wachter, 2008). Sistemic toxicity is low, even if phototoxic reactions have been described.
An interesting therapeutic option is represented by topical imiquimod. It enhances the immune system activity leading to an induction of melanoma-specific cytotoxic T-cells by cross presentation of melanoma antigen by dendritic cells. Partial remission of locoregional cutaneous metastases treated with imiquimod was demonstrated (Wolf, Richtig, Kopera & Kerl H, 2004).
Skin metastases from melanoma are a frequent finding in the natural history of the disease with various clinical, morphological and histopathologic backgrounds. The presence of progressively increasing metastases is often distressing for the patient, and ulceration, bleeding and super-infections can negatively impact on the life-quality. To date, many treatments are available for the clinical management of these lesions. Thus, clinicians should be informed about the prognostic implications and the therapeutic options in order to choose the best cost-effectiveness treatment modality.
Ascites is a term used to describe the condition of accumulation of fluid in the peritoneal cavity. The word “ascites” could be used interchangeably with other terms such as abdominal dropsy, abdominal effusion, peritoneal fluid excess, hydroperitoneum and peritoneal cavity fluid. Ascites represents a form of general systemic state which could manifest in diverse disease conditions in animals. This implies that ascites is only a clinical manifestation of an underlying disease condition and not a disease in real sense. It further shows that ascites is not a treatable condition except the cause is properly diagnosed and treated accordingly. Ascites is often diagnosed in dogs between the ages of 5 and 7 years [1]. Cases between the ages of 1 and 4 years have also been recorded. The occurrence of ascites in dogs may be breed dependent with higher incidences in Pomeranian (33.35%) than in Labrador retriever (20%), Boxer (16.66%), Doberman pinscher (13.37%), mongrels (10%) and least in Alsatian (6.66%) [1]. Ascites manifests in several disease conditions such as hepatic disease, various types of neoplasm, portal hypertension, alteration in serum protein level (hypoproteinaemia), right-sided heart failure, decreased plasma oncotic pressure and increased permeability of capillary endothelium sequel to inflammatory conditions, bacterial infection (tuberculosis), kidney malfunction, pre-hepatic portal hypertension, post-hepatic portal hypertension, trauma (rupture of lymphatic vessels, blood vessels, urinary bladder),
ancylostomosis peritonitis, bleeding disorders and malnutrition [2, 3]. Other conditions may include heartworm infection and pulmonary stenosis [4]. In general, cardiac and hepatic disease conditions ranked highest as the cause of ascites in pets. Other manifesting signs which usually signify an underlying disease condition in ascetic pets may include syncope, vomiting, obtundation, seizure, anaemia which manifests as pale mucous membrane, weakness and rapid panting. The identification and diagnosis of the cause of ascites may not be a straightforward procedure and could be complicated due to the several causative factors. The veterinarian however has to be guided by the medical adage “if you hear the sound of hoof first look for a horse before a zebra”. This only means that diagnosis should start with the basis of thorough physical examination of the entire body and clinical examinations. A well and sequential conduction of physical and clinical examinations serves as a pointer to the underlying cause of ascites. However this may not always be so as diagnosis oftentimes is cumbersome. In such situations diagnosis would include a complete blood count which may reveal evidence of bacterial infection. Abdominal ultrasound/sonography is done to determine the abdominal content and aid in differentiating excess fluid accumulation from abdominal masses and organ enlargement. Knowledge of the blood biochemistry including total protein, albumin, creatinine and urea, liver enzymes and coagulation profile would help in revealing cases of hypoalbuminaemia, hypoproteinaemia and hepatic and kidney diseases [5]. Cardiac diseases may be diagnosed with the aid of electrocardiograph. Cardiac auscultation detects cases of cardiac murmurs and arrhythmia. Abdominal paracentesis is a useful procedure usually carried out to reduce the fluid level and alleviate complications of dyspnea. Paracentesis is a useful procedure in the management of ascites which is instituted in conjunction with appropriate treatment of the underlying cause. Once appropriate diagnosis is made, treatment usually comes easy by alleviating life-threatening conditions such as dyspnea and administering appropriate therapy as the case may be.
The purpose of this review is primarily focused on the various causes of ascites with emphasis on the hepatic origin. Based on this premise, ascites is classified broadly into hepatic, pre-hepatic and post-hepatic origin:
Pre-hepatic causes emanate from portal vein thrombosis, bacterial infection such as tuberculosis, malnutrition, hypoalbuminaemia and parasitic diseases such as strongyloidosis and entamoeba [6]. Other causes include trauma or rupture of the lymphatic vessels, blood vessels and urinary bladder, renal failure, lymphoma and neoplasm of various kinds including breast, bronchus, ovary, gastric, pancreatic or colonic neoplasms [7]. Up to 20% of neoplastic ascites arise from tumour of unknown origin [7].
Post-hepatic causes might include congestive heart failure often linked with pulmonary hypertension, left-sided heart failure, right-sided heart failure, constrictive pericarditis, Budd-Chiari syndrome and stricture web formation in the inferior vena cava [8, 9].
Hepatic origin emanates from various hepatic diseases including cirrhosis, portal hypertension and hepatitis. Approximately 85% of portal hypertension results in cirrhosis [8, 9, 10].
Earlier classification of ascites was centred on two broad categories, transudates and exudates, based on the total protein concentration of ascetic fluid. High total protein (>2.5 g/l) was described as exudates, while low total protein (<2.5 g/l) as transudate [11]. Both transudates and exudates were subcategorised into modified transudates and exudates based on the level of total protein concentration in the ascetic fluid. Transudates with <2.5 g/l of total protein usually occur with portal hypotension or hypoalbuminaemia [6]. Exudates with >2.5 g/l of total protein are associated with inflammatory disease conditions such as bacteria tuberculosis, neoplasm of unknown origin, pancreatitis, myxoedema, etc. Nevertheless, it has been observed that a total protein concentration of <2.5 g/l has an accuracy of only 56% [6] in detecting exudates from various conditions such as cardiac ascites and patients on diuretics and neoplasms [11]. The obvious challenge in the use of total protein concentration paved way to the discovery of serum ascites albumin gradient (SAAG) concentration as a more reliable tool in classification of ascites with efficacy ranging from 80 to 100% [11]. With the advent of SAAG, exudate ascites is replaced with (>1.1 g/l) high serum ascites albumin gradient and transudate with low (<1.1 g/l) serum ascites albumin gradient. The SAAG (>1.1 g/l) shows higher 94% sensitivity and 90% specificity in detecting portal hypertension than ascetic fluid total protein concentration of <2.5 g/dl at percentage sensitivity and specificity of 78 and 50%, respectively [12]. The prognostic index value of SAAG was at 82–97% compared to total protein concentration at 38–85% [12]. Ascites from cardiac origin produces greater(>2.5g/dl) SAAG compared to cases of cirrhosis [13].
A more recent classification of ascites has endorsed the use of serum ascites albumin gradient (SAAG) in diagnosis of ascites [14]. The SAAG is derived by subtracting the ascetic fluid albumin level from the serum albumin level obtained on the same day [14]. Gradients greater than 1.1 g/dl indicate ascites of portal hypertension with an accuracy of 97–100% [14]. Gradients less than 1.1 g/dl are considered ascites of other sources other than portal hypertension such as neoplasm [15, 16] (Table 1).
High gradient (>1.1 g/l) SAAG | Low gradient (<1.1 g/l) SAAG |
---|---|
Portal hypertension | Bacterial infection |
Cardiac diseases | Peritoneal tuberculosis |
Liver cirrhosis | Pancreatic ascites |
Myxoedema | Parasitic disease |
Budd-Chiari syndrome | Ancylostomosis |
Hepatitis | Nephrotic syndrome |
Portal vein thrombosis | Trauma and rupture of lymphatic and blood vessels |
Hypoalbuminaemia | Rupture of the urinary bladder, left-sided heart failure, right-sided heart failure, congestive heart failure |
Classification of ascites based on SAAG.
Ascites is one of the cardinal complications in liver cirrhosis in most patients [8]. Onset of ascites naturally connotes decompensated underlying liver cirrhosis which also signifies poor prognosis with short life expectancy [10, 17, 18]. Several factors contribute to the development of cirrhosis. The heart, for instance, plays an important role through a complex mechanism in the development of liver disease. The mechanism through which the heart and liver affect each other in the development of ascites is yet to be fully elucidated [14]. Several circulatory abnormalities observed in cirrhotic patients promulgated the peripheral arterial vasodilation hypothesis proposed in the last century [19]. The circulatory abnormalities manifest as increased cardiac output, portal hypertension, peripheral vascular resistance, arterial hypotension and splanchnic vasodilation [6, 20]. Circulatory abnormalities from cardiac disease affect circulatory volume with a resultant decrease in tissue perfusion affecting majorly the kidney functionality [21]. Earlier in the disease, renal dysfunction is less expressed; however, with disease advancement the patient may experience difficulty in sodium excretion and consequent sodium and water retention [22]. Cirrhotic ascites basically develop from failure in renal excretion of sodium [22]. Different mechanisms also play a role in ascites in cirrhosis. Intrinsic factors including arterial vasodilation affect the blood pressure hormones such as the renin-angiotensin-aldosterone system (RAAS) which stimulates sodium reabsorption from the distal nephron [22]. The sympathetic nervous system (SNS) induces renal constriction and sodium reabsorption from the tubules with ascites [23, 24]. The heart, SNS and RAAS play a synergistic role in sodium retention and development of ascites in cirrhosis.
The portal vein is a major vein comprising of a group of veins which supply the visceral organs including the abdomen, pancreas, intestine, etc. These veins bifurcate into smaller vessels in the hepatic tissue. Intrinsic factors and disease conditions such as cirrhosis result in blockage of these tiny veins in the hepatic tissue increasing the blood pressure in the veins with resultant portal hypertension. Other causes of portal hypotension include portal vein thrombosis, schistosomosis, idiopathy, etc. Ascites develops in portal hypertension when the post-sinusoidal gradient is above 12 mmHg [25]. Portal hypertension elevates the hydrostatic pressure within the hepatic sinusoids permitting seepage of transudate into the peritoneal cavity [26, 27]. The extent of ascites’ development is dependent on the level of hydrostatic pressure [28] and less on oncotic plasma albumin pressure [26, 29]. Signs and symptoms of portal hypertension include haematuria, dysentery, bloody vomitus due to spontaneous rupture and haemorrhage from varices, encephalopathy due to abnormal liver function and thrombocytopaenia. Factors such as abnormal increase in nitric oxide production and circulation of endogenous vasoconstriction such as catecholamines, leukotrienes and angiotensin II enhance hepatic vascular resistance and portal hypertension [30, 31].
One of the complications of activation of RAAS and SNS in cirrhosis is the resultant renal vasoconstriction leading to decrease in renal perfusion and glomerular filtrate rate which progresses to renal impairment [21, 22, 32, 33]. In hepatorenal syndrome, there are no significant morphological changes in renal histology, while the patients largely retain normal tubular function [5, 21]. The kidney analyte and serum creatinine concentration does not increase until the glomerular filtration rate becomes markedly reduced below 40 ml/min [22]. Most patients with cirrhosis have their creatinine level below 1.2 mg/dl, and diagnosis of HRS is only made when the creatinine concentration is higher than 1.5 mg/dl in the absence of other complicating aetiologies [22]. Hepatorenal syndrome manifests in two different types in cirrhotic patients. Type I HRS is a fulminating form of the disease rapidly progressing to acute renal failure often precipitated by variceal bleeding, septic infection and spontaneous bacteria peritonitis with poor prognosis of days to weeks [22]. Type 2 is a more chronic form of HRS. Most patients with this form of disease have a more stable creatinine concentration with only signs of refractory ascites due to unresponsive diuretics [34, 35].
With advancement in cirrhosis, there is also progressive increase in sodium and water reabsorption and decrease in renal blood flow and glomerular filtration [36]. Approximately 20% of cirrhotic patients with refractory ascites progress to HRS which results from severe liver and systemic circulatory dysfunction [28]. Hepatorenal syndrome results from marked overactivity of RAAS, SNS, AND and other endogenous vasoconstrictor factors which exceeds renal production of vasodilatory substances [PGE2, prostacyclin, nitric oxide]. The imbalance from renal vasodilatory mechanism and the intrinsic vasoconstrictor enhances vasoconstriction and hypoperfusion and decreases GFR with ultimate result of renal failure [22].
Usually there is no laid down procedure on the steps to diagnose ascites; however a systematic approach applied in various disease conditions is advantageous in making appropriate diagnosis. A step-by-step approach normally starts with physical examination.
In physical examination, the patient is examined for the presence of ticks and fleas which would contribute in physical discomfort of the pet. Ticks’ infestation contributes in depletion of blood volume and anaemia. Anaemia is detected by the appearance of pale mucous membrane of the eye and the gum. Ectoparasitism from ticks’ infestation may result in malnutrition due to competition with the host for essential nutrients necessary for the synthesis of protein and albumin. This could result in hypoalbuminaemia/hypoproteinaemia and a decrease in plasma oncotic pressure enhancing vascular permeability and seepage of fluid in the abdominal cavity. A distended or pulsating jugular vein in the neck region may indicate cardiovascular abnormality. Yellowish discoloration of the eye indicates jaundice and hepatic disease. Generalised lymphadenopathy may suggest lymphosarcoma and other inflammatory disease conditions. A “standback” observation reveals cases of dyspnea due to abdominal displacement of the diaphragm into the thoracic cavity compromising respiration. Respiratory distress could manifest in the form of rapid panting. Such condition presents a deviation from the normal respiratory pattern, from coastal to costo-abdominal or abdominal pattern. Black tarry-coloured faeces from gastrointestinal bleeding may signify ancylostomosis and portal hypertension. Physical examination of the trunk reveals a distended abdomen. The content of the abdomen could either be by pregnancy, abdominal masses, fluid of various consistencies or organ enlargement. The diagnosis of ascites starts from differentiating these possibilities through various procedures. First is to carry out abdominal ballottement using clinched fist. This technique can be used to differentiate abdominal masses from fluid. It can be used with other laboratory tests such as pregnancy test to rule out pregnancy. It however has some limitations in differentiating abdominal masses from organ enlargement. Abdominal ultrasound is a better option in differentiating abdominal contents. It has been proven effective in the detection of ascetic fluid, its site of production and differentiation of ascetic nature from transudates and exudates [11]. A recent research has shown the possibility of the use of echotexture of ascetic fluid in the detection of the cause of ascites in patients [11]. Abdominal paracentesis however is a very useful technique in differentiation of ascetic fluid [28].
A well-applied paracentesis without contamination of abdominal content is essential in differentiation of ascetic fluid. To achieve this, the following steps should be strictly applied:
First apply caution by the use of proper restrain technique on the dog.
Gently place the dog on a lateral decumbency exposing the larger part of the ventral abdomen.
Swab the ventral abdomen less covered with haircoat, along the linea alba down to the ventral abdomen between the left and right hindlimbs. (Linea alba is the preferred site of paracentesis due to its less vascularisation and less chance of contamination of the fluid with blood from puncture vessels and abdominal organs when approached through a different site on the abdomen.)
Puncture the linea alba using a 21 gauge needle and 10 mL gauge syringe, and aspirate the fluid.
Decant the content of the syringe into a clean and well-labelled tube for laboratory investigation.
Request for cytology of the fluid (Figure 1).
Removal of ascites through the linea alba in an Alsatian breed of dog.
The colour of ascetic fluid is a very essential marker in the diagnosis of the cause of ascites. The colour ranges from clear fluid to yellowish, reddish and opaque with flakes of fibrin and debris depending on the aetiology. It is therefore important to observe the above guidelines in paracentesis in order to avoid false discolouration of the fluid, thus affecting correct diagnosis. Various colours of ascetic fluid signify a different aetiology as shown below [37]:
Pinkish discolouration of the fluid: This is often seen in cases of exudation of fluid from bacterial infection which may become purulent. The exudates are often turbid in consistency and contains more than 2.0 gm of protein and greater than 6000 cells/μL composed mostly of neutrophils with evidence of +++ bacterial infection. This type of fluid is considered a medical emergency to prevent development of sepsis.
Clear straw-coloured fluid: This type of fluid is described as modified transudate often characterised by the presence of fibrin cells and white blood cells such as neutrophils and lymphocytes. It is often seen in cases of long-standing ascites from various conditions including right-sided heart failure, cancerous growth and hepatic disease giving chance to invasion of fibrinogens.
Clear opaque fluid: This fluid is described as collection of pure transudate into the peritoneal cavity free from contamination except with few invasions of mesothelial cells and tissue macrophages. This ascites may be seen in cases of portal hypertension, hepatic diseases, osmotic gradient deficit (hypoalbuminaemia), protein losing enteropathy, kidney impairment and albuminuria.
Reddish discolouration of fluid: This is seen in cases of haemorrhages and collection of frank blood in the peritoneal cavity due to conditions of trauma, coagulopathies and blood and blood vessel neoplasm. The fluid contains high levels of cells mainly red blood cells with PCV being above 20%.
Greenish discolouration of fluid: This is seen in cases of rupture and seepage of bile into the peritoneal cavity.
Milky/slightly yellowish discolouration: This describes a condition of collection of lymph in the peritoneal cavity due to trauma, infection, cancer or right-sided heart failure. This type of exudates is turbid and opaque and is often described as chyle. It gives a positive result in Sudan III stain test for lipids due to the high level of lipid in the fluid.
Clinical examination is considered a useful tool in the identification of the cause of ascites. An elevated temperature would signify an underlying infectious or inflammatory condition such as bacterial tuberculosis. An elevated capillary refill time would signify a decreased circulatory volume as a result of cancerous or infectious condition. Auscultation of the heat reveals various cardiovascular diseases such as muffled heart sound which is consistent with pericardial effusion and cardiac tamponade. Heart murmurs or irregular heartbeats are suggestive of right-sided heart failure. An elevated heartbeat or tachypnoea may result from dyspnea due to cranial displacement of the diaphragm into the thoracic cavity. Cardiovascular abnormalities are confirmed through the use of electrocardiograph and echocardiography.
The determination of biochemical profile such as the liver enzymes, total protein level, SAAG, albumin concentration, total bilirubin and kidney analytes such as creatinine and urea levels is useful in the diagnosis of the cause of ascites.
Serum ascites albumin gradient is presently the best tool in diagnosis of the cause of ascites especially that from portal hypertension [38]. A SAAG value of <1.1 g/dl or 11 g/l indicates causes of non-portal origin such as malignancy, etc. [5]. Gradients >1.1 g/dl or 11 g/l indicate ascites of portal hypertension.
Although the traditional classification of ascites according to the transudate and exudate concept has almost phased out following the introduction of SAAG, it however still has relevance in clinical practice for comparison and prognostic value. Concentrations below 15 g/l are often associated with risk of spontaneous bacteria peritonitis in cirrhosis [5, 39].
An elevated triglyceride concentration in ascetic fluid above 2.2 mmol/l indicates chylous ascites [38]. Chylous ascites is common in neoplastic cases although it may occur in 6% of cirrhosis [40].
Elevated levels in urea and creatinine concentrations in ascetic fluid indicate prerenal failure due to peritoneal absorption of urea [41]. Urinary ascites is often associated with bladder changes and urethra obstruction [41, 42].
Cytology of ascetic fluid is often indicated in suspected malignancy and idiopathic cases. Positive cytology is highly indicated in suspected cases of peritoneal carcinomatosis. The sensitivity of cytology can be enhanced by examination of three samples from separate paracenteses [38]. The sensitivity is also enhanced by prompt analysis of ascetic fluid and obtaining large volume of up to 50–1000 ml in patients with initial negative result.
Diagnostic laparotomy is indicated in cases of difficulty in identification of the aetiology of ascites. Often laparotomy presents adequate visual inspection of the peritoneal cavity and avenue for biopsy collection for histological and microbiological studies [38]. Diagnostic laparotomy provides ground for effective diagnosis of peritoneal carcinomatosis, tuberculous peritonitis, etc. [43, 44].
Several studies have shown the usefulness in the use of leucocyte esterase reagent strip in diagnosing spontaneous bacteria peritonitis and in urinary analysis with sensitivity ranging from 80 to 93% and specificity 93–98% [45]. The negative predictive value is markedly high from 97 to 99%, a good measure for an ideal tool to rule out SBP [45]. Recent development has discovered an ascite-specific reagent strip with a cut-off value of 250 cells/mm3 which would further enhance diagnostic accuracy [46].
Increased platelet indices such as mean platelet volume and platelet distribution width have been observed to increase in cirrhosis. The usefulness of the platelet indices is yet to be fully elucidated but has shown propensity as a potential diagnostic tool [47].
The use of tumour markers such as alpha - feto protein, des-gamma-carboxy prothrombin, cancer antigen 125, etc. in the diagnosis of cancer in ascetic fluid is presently a subject of controversy among several researchers. Although the increased level of these markers is associated with underlying malignancies, elevated levels are also observed in other conditions such as pancreatitis, gastritis, etc. [48].
Radiographical imaging is useful in detailing small amounts of ascetic fluid as well as diagnosis of aetiology of ascites [49]. Abdominal ultrasonography can detect as little as 100 ml of intraperitoneal fluid [50]. The sensitivity of radiography is enhanced through the use of computed tomography which detects minute quantities of ascetic fluid. Radiography enhances the picture of internal organs and aids in detection of cirrhosis, intra-abdominal tumour and organ enlargements. Thickening of mesentery and bowel wall, matting of bowel loops and enlargement of mesenteric lymph nodes may provide a guide in the diagnosis of tuberculosis peritonitis in affected patients. A contrast computed tomography (CT) may be used to demonstrate enhancement of peritoneal lining. Cases of cirrhosis and large hydrothorax can be diagnosed with the aid of scintigraphy with technetium sulphur colloid or radiolabelled albumin [6].
Spontaneous bacterial peritonitis may arise due to decreased level of compliments which serve as antibacterial factors in ascetic fluid. Suspected cases of SBP are cultured in both aerobic and anaerobic blood media for isolation of organisms [51]. Cultured ascetic fluid should be subjected to sensitivity test to identify effective antimicrobiological agent in treatment.
The DNA of Mycobacterium tuberculosis in ascetic fluid can be detected using polymerase chain reaction in suspected cases. PCR for Mycobacterium tuberculosis offers a high sensitivity (94%) test compared to microscopic acid-fast bacilli smear (−0%) and mycobacterial culture (−50) [38].
Ascites is treated symptomatically while addressing the primary cause of the condition. Efforts are geared towards relieving manifesting symptoms and preventing progression of ascites. The main goal in congestive heart failure is to improve cardiac contractility, normalise cardiac arrhythmias and enhance cardiac output. Cardiac drugs such as dopamine and digoxin can be used at recommended dosages in cases of congestive heart failure in dogs. Dogs with right-sided heart failure should be placed on cage rest and on sodium-restricted diet [52]. Paracentesis is applied to relieve abdominal tension on the diaphragm and enhance normal respiration. Repeated paracentesis is not required except in cases of failing treatment [52]. Paracentesis should not exceed 1.0 kg weight per day for dogs with both ascites and peripheral oedema and less than 0.5 kg weight per day for patients with only ascites. Serum albumin sometimes is depleted during paracentesis and therefore should be monitored and replaced intravenously in case of depletion at the same quantity of fluid removed. The administration of albumin dosed at 1.5 g/kg on the first day and 1.0 g/kg on the third day ensured renal preservation and reduced mortality [53]. In cases of syncope, a balanced isotonic crystalloid fluid replacement such as Plasma-Lyte A, Normosol R and 0.9% saline may be used in resuscitation and other conditions such as hypernatraemia, hyponatraemia, hypercalcemia, metabolic alkalosis or oliguria renal failure. Diuretics are used in addition to paracentesis to relieve ascites. Diuretics may be dosed once daily. Spironolactone has a half life of 24 hours and is given at the dose of 100 mg/day max 400 mg/day for response [54]. The dose may be spread out every 2 hours stat in dogs under hospitalisation and close monitoring at 2 mg/kg × im and at 3 mg/kg × per os at night. Spironolactone could be substituted with either triamterene or amiloride since both drugs have good antagonistic effect on aldosterone action on the collecting tubules [55]. Furosemide is often the first line of treatment in cases of ascites with a half life of 1.5 hours and given at the dose of 40 mg/day and max 160 mg/ day in case of nonresponders to furosemide [39]. The dose may also be spread in divided doses of 3 mg/kg × IV every 2 hours and at 4 mg/kg per os at night. Bumetanide and spironolactone could be used in combination with furosemide at the ratio of 100:40 to reduce chances of furosemide resistance. The dose ratio ensures efficient natriuresis and flow of water and also reduces the risk of potassium deficit from the use of furosemide [39, 56]. Other diuretics such as torsemide and bumetanide have shown better efficacy than most diuretics [57]. Torsemide has a longer half life than both furosemide and bumetanide [57]. Patient with cirrhotic ascites often presents with complications of SBP, portal hypertension and HRS [28]. Cases without such complications are described as “uncomplicated ascites” [58]. The standard treatment for SBP in humans involves immediate administration of third-generation cephalosporin such as intravenous ceftriaxone 1 to 2 g daily for 5 days [52]. The dose could be given at 1 g daily in dogs. The use of oral fluoroquinolones is equally effective in the treatment of SBP [59, 60]; alternatively piperacillin and tazobactam could be considered [61]. The choice of antibacterial agent depends on culture and sensitivity test to reduce problems of drug resistance. Antibiotic treatment is usually given for an extended period to ensure complete cure of the bacterial infection.
Portal hypertension is managed by the use of antihypertensive medications. A drug such as metolazone (Mykron, Zaroxolyn) aids in the elimination of oedema in congestive heart failure. It enhances sodium excretion by inhibition of sodium reabsorption from the distil tubules, a function which is beneficial in renal conditions [55]. Mannitol (Osmitrol) inhibits tubular reabsorption of electrolyte by increasing the osmotic pressure of glomerular filtrate and urine output [55]. Cases of recurrent ascites in humans from portal hypertension may require the use of TIPS [28]. TIPS functions as a side-to-side portacaval anastomosis between the high portal pressure end and low hepatic vein pressure end, thereby effectively decongesting the portal system which may be useful in pets. A reduction in the portal hypertension brings a secondary decrease in RAAS activation and consequent increase in sodium excretion [62]. Persistent ascites from cirrhosis may be managed through liver transplant and removal of the damaged liver. The hepatic cells naturally possess high regenerative capacity and can regenerate after undergoing severe degenerative condition. The hepatocytes in addition can perform at full capacity even with few viable cells, and therefore liver transplant is only required as a last resort after application of all remedial medications.
Renal failure is managed by controlling blood pressure with drugs; avoid the use of hepatotoxic medications in treatment of ascites and the use of non-steroidal anti-inflammatory agents (NSAIDs) such as acetaminophen. Kidney dialysis is recommended in severe kidney damage. A continuous venovenous haemodialysis (CVVHD) is recommended compared to intermittent renal dialysis.
Cases of complications of encephalopathies from hepatic failure are best managed in intensive care units (ICU) [18]. Cases of early complication of encephalopathy may be treated as outpatient; nevertheless such a patient is closely monitored for further deterioration to grade II encephalopathy which would require prompt transfer to an intensive care unit. Such a patient is placed on routine check on mental balance, and signs of restlessness could be slightly sedated with low dose of short-acting benzodiazepines. Patients under sedation are placed on undisturbed bed rest avoiding extensive movement which may enhance chances of intracranial pressure/hypertension. Dyspnea is prevented in late encephalopathy through placement of intratracheal intubation to avoid further complications of aspiration pneumonia. The conditions of cerebral oedema and intracranial hypertension manifest at the late phase of encephalopathy and are prevented through routine checks on the patient’s renal parameters; biochemical profile including liver enzymes, total protein, glucose, electrolytes and acid/balance; and neurological evaluations for signs of elevated levels [4]. Cases of severe bleeding result from problems of coagulopathies which can be treated by addressing the coagulopathy through transfusion of coagulation products such as fresh frozen plasma and platelets and administration of vitamin K. Severe conditions may be boosted by transfusion of packed red blood cells. Continuous bleeding after massive replacement infusions may indicate possible retroperitoneal bleeding [18]. A good number of herbal and antioxidant medications have shown to be beneficial in the treatment of ascites of hepatic origin. The use of these drugs remains controversial, but despite this the drug N-acetylcysteine and Silybum marianum still remain the drug of choice in the treatment of hepatic damage from acetaminophen toxicity and hepatic dysfunction, respectively [63].
Conclusion: Ascites is a disease condition commonly seen in pets of various age brackets with high incidences occurring in middle-aged dogs. Ascites is a common manifestation of a decompensate cirrhosis, cardiac diseases and several other aetiologies and is best diagnosed through established standard procedures of physical and clinical examinations, complete blood picture, cytology and various biochemical analyses. Recent novel techniques such as platelet indices, leucocyte esterase reagent strip, tumour markers, bacterial DNA, cytokines and other proteins are available for the advancement of biochemical laboratory techniques and efficient diagnosis of ascites. Treatment is centred on effective diagnosis of the aetiology.
I sincerely acknowledge the God Almighty for His enablement bestowed upon me during the course of this write-up.
difficulty in breathing degenerative condition in the brain obstruction of the bile duct red blood cell destruction study of both the stomach and intestines study of the blood study of the nervous tissues accumulation of fluid in the abdominal cavity accumulation of fluid in the abdominal cavity irregular heartbeat closure or blockage especially to stop bleeding problem with blood clotting mechanism reversibly combined with a compound compound in its natural form not transparent, cloudy, filmy the cause of a disease condition area supplied with blood vessels fluid produced from increased pressure in the hepatic, portal vein (>8 mmHg) usually around 20 mmHg, low in protein (<30 g/L), low in LDH, high pH, normal glucose and fewer cells fluid actively secreted from inflammation or malignancy, rich in protein, lactate dehydrogenase, low pH (<7.30), low glucose level and large numbers of white blood cells pertains to the kidney condition that affects both the liver and kidney active compound in milk thistle herbal preparation a poisonous species of mushroom unknown origin
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