Principles of Surgical Resection of Hepatocellular Carcinoma
INTRODUCTION
There has been significant improvement in the perioperative results following liver resection, mainly due to techniques that help reduce blood loss during the operation. Extent of liver resection required in HCC for optimal oncologic results is still controversial. On this basis, the rationale for anatomically removing the entire segment or lobe bearing the tumor, would be to remove undetectable tumor metastases along with the primary tumor.
SIZE OF TUMOR VERSUS TUMOR FREE-MARGIN
Several retrospective studies and meta-analyses have shown that anatomical resections are safe in patients with HCC and liver dysfunction, and may offer a survival benefit. It should be noted, that most studies are biased, as non-anatomical resections are more commonly performed in patients with more advanced liver disease, which affects both recurrence and survival. It therefore remains unclear whether anatomical resections have a true long-term survival benefit in patients with HCC. Some authors have suggested that anatomical resections may provide a survival benefit in tumors between 2 and 5 cm. The rational is that smaller tumors rarely involve portal structures, and in larger tumors presence of macrovascular invasion and satellite nodules would offset the effect of aggressive surgical approach. Another important predictor of local recurrence is margin status. Generally, a tumor-free margin of 1 cm is considered necessary for optimal oncologic results. A prospective randomized trial on 169 patients with solitary HCC demonstrated that a resection margin aiming at 2 cm, safely decreased recurrence rate and improved long-term survival, when compared to a resection margin aiming at 1 cm. Therefore, wide resection margins of 2 cm is recommended, provided patient safety is not compromised.
THECNICAL ASPECTS
Intraoperative ultrasound (IOUS) is an extremely important tool when performing liver resections, specifically for patients with HCC and compromised liver function. IOUS allows for localization of the primary tumor, detection of additional tumors, satellite nodules, tumor thrombus, and define relationship with bilio-vascular structures within the liver. Finally, intraoperative US-guided injection of dye, such as methylene-blue, to portal branches can clearly define the margins of the segment supplied by the portal branch and facilitate safe anatomical resection.

The anterior approach to liver resection is a technique aimed at limiting tumor manipulation to avoid tumoral dissemination, decrease potential for blood loss caused by avulsion of hepatic veins, and decrease ischemia of the remnant liver caused by rotation of the hepatoduodenal ligament. This technique is described for large HCCs located in the right lobe, and was shown in a prospective, randomized trial to reduce frequency of massive bleeding, number of patients requiring blood transfusions, and improve overall survival in this setting. This approach can be challenging, and can be facilitated by the use of the hanging maneuver.

Multiple studies have demonstrated that blood loss and blood transfusion administration are significantly associated with both short-term perioperative, and long-term oncological results in patients undergoing resection for HCC. This has led surgeons to focus on limiting operative blood loss as a major objective in liver resection. Transfusion rates of <20 % are expected in most experienced liver surgery centers. Inflow occlusion, by the use of the Pringle Maneuver represents the most commonly performed method to limit blood loss. Cirrhotic patients can tolerate total clamping time of up to 90 min, and the benefit of reduced blood loss outweighs the risks of inflow occlusion, as long as ischemia periods of 15 min are separated by at least 5 min of reperfusion. Total ischemia time of above 120 min may be associated with postoperative liver dysfunction. Additional techniques aimed at reducing blood loss include total vascular isolation, by occluding the inferior vena cava (IVC) above and below the liver, however, the hemodynamic results of IVC occlusion may be significant, and this technique has a role mainly in tumors that are adjacent to the IVC or hepatic veins.

Anesthesiologists need to assure central venous pressure is low (below 5 mmHg) by limiting fluid administration, and use of diuretics, even at the expense 470 N. Lubezky et al. of low systemic pressure and use of inotropes. After completion of the resection, large amount of crystalloids can be administered to replenish losses during parenchymal dissection.
LAPAROSCOPIC RESECTIONS
Laparoscopic liver resections were shown to provide benefits of reduced surgical trauma, including a reduction in postoperative pain, incision-related morbidity, and shorten hospital stay. Some studies have demonstrated reduced operative bleeding with laparoscopy, attributed to the increased intra-abdominal pressure which reduces bleeding from the low-pressured hepatic veins. Additional potential benefits include a decrease in postoperative ascites and ascites-related wound complications, and fewer postoperative adhesions, which may be important in patients undergoing salvage liver transplantation. There has been a delay with the use of laparoscopy in the setting of liver cirrhosis, due to difficulties with hemostasis in the resection planes, and concerns for possible reduction of portal flow secondary to increased intraabdominal pressure. However, several recent studies have suggested that laparoscopic resection of HCC in patients with cirrhosis is safe and provides improved outcomes when compared to open resections.
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Resections of small HCCs in anterior or left lateral segments are most amenable for laparoscopic resections. Larger resections, and resection of posterior-sector tumors are more challenging and should only be performed by very experienced surgeons. Long-term oncological outcomes of laparoscopic resections was shown to be equivalent to open resections on retrospective studies , but prospective studies are needed to confirm these findings. In recent years, robotic-assisted liver resections are being explored. Feasibility and safety of robotic-assisted surgery for HCC has been demonstrated in small non-randomized studies, but more experience is needed, and long-term oncologic results need to be studied, before widespread use of this technique will be recommended.
ALPPS: Associating Liver Partition with Portal vein ligation for Staged hepatectomy

The pre-operative options for inducing atrophy of the resected part and hypertrophy of the FLR, mainly PVE, were described earlier. Associating Liver Partition with Portal vein ligation for Staged hepatectomy (ALPPS) is another surgical option aimed to induce rapid hypertrophy of the FLR in patients with HCC. This technique involves a 2-stage procedure. In the first stage splitting of the liver along the resection plane and ligation of the portal vein is performed, and in the second stage, performed at least 2 weeks following the first stage, completion of the resection is performed. Patient safety is a major concern, and some studies have reported increased morbidity and mortality with the procedure. Few reports exist of this procedure in the setting of liver cirrhosis. Currently, the role of ALPPS in the setting of HCC and liver dysfunction needs to be better delineated before more widespread use is recommended.
Anatomia Cirúrgica Hepática

INTRODUÇÃO
O fígado, o maior órgão interno do corpo, representa aproximadamente 2-3% do peso corporal total de um adulto. O conhecimento preciso da arquitetura do fígado, do trato biliar, dos vasos sanguíneos relacionados e da drenagem linfática é essencial para o sucesso da cirurgia hepatobiliar, incluindo o transplante de fígado.
LIGAMENTOS HEPÁTICOS | MEIOS DE FIXAÇÃO
O fígado é completamente coberto por uma cápsula de Glisson (tecido conjuntivo denso não modelado) e envolto por peritônio, exceto em sua superfície posterior, que envolve três estruturas principais no hilo hepático: a artéria hepática, a veia porta e o ducto biliar. Os ligamentos são dobras do peritônio que sustentam o fígado. Alguns exemplos incluem o ligamento redondo (ligamento teres), o ligamento falciforme, o ligamento coronário, os ligamentos triangulares direito e esquerdo, e o ligamento venoso (ligamento de Arantius). O fígado é suspenso por anexos fibrosos (ligamentos) e veias hepáticas, exceto na área nua onde se conecta ao diafragma. O peritônio parietal forma duas camadas que continuam no ligamento falciforme e envolvem o fígado, exceto na área nua, onde se separam para formar o ligamento coronário e o ligamento triangular esquerdo. A camada esquerda do ligamento falciforme se torna a camada superior do ligamento coronário esquerdo, enquanto a camada direita se torna a camada superior do ligamento coronário direito, que se une à camada inferior para formar o ligamento triangular direito. A camada inferior do ligamento coronário continua na superfície posterior do fígado e pode se refletir na parte superior do rim direito para formar o ligamento hepatorrenal. Em seguida, ele passa pela frente do sulco da veia cava inferior (VCI) e, após um curso semicircular na frente do lobo caudado, encontra a folha direita do omento menor. A folha do omento menor continua na folha posterior do ligamento triangular esquerdo.
LIGAMENTO VENOSO
Este é o remanescente do canal de Arantius (ductus venosus), que transporta sangue oxigenado da veia umbilical esquerda através da veia porta esquerda até o átrio direito durante a vida fetal. Após o nascimento, o ducto se oblitera e persiste como o ligamento venoso ou ligamento de Arantius. O ligamento de Arantius geralmente se insere na veia hepática esquerda ou no sulco entre as veias hepáticas média e esquerda. O ligamento pode ser isolado, puxado para cima e para a esquerda, e utilizado para separar as veias quando é necessário controlar a veia hepática esquerda. Esta manobra é útil para passar um laço vascular ao redor da veia hepática esquerda para colher um enxerto do segmento lateral esquerdo em transplante de fígado doador vivo ou na divisão do segmento lateral esquerdo in situ. Com dissecção adicional, a manobra pode ser usada para circundar o tronco comum das veias hepáticas esquerda e média para preparar a colheita do fígado esquerdo em transplante de doador vivo ou de fígado dividido, ou para a oclusão seletiva da veia hepática durante ressecções hepáticas. No lado portal, cortar a origem do ligamento próximo à veia porta (ou seja, quando a veia é liberada do umbilical e da placa transversa) é uma manobra chave para ganhar comprimento na veia porta esquerda (na hepatectomia do doador à esquerda, ou durante a hepatectomia à direita junto com a ressecção da bifurcação da veia porta em colangiocarcinoma perihilar), ou exposição na placa umbilical (na operação de Kasai).
LIGAMENTO HEPATOCAVAL
A borda posterior do lobo caudado à esquerda possui um componente fibroso (o ligamento hepatocaval ou ligamento dorsal ou ligamento de Makuuchi) que se fixa ao cruzamento do diafragma e se estende posteriormente atrás da veia cava inferior para se unir ao segmento VII no lado direito da veia cava. Em uma grande proporção de pacientes, este tecido fibroso é substituído pelo parênquima hepático, total ou parcialmente, e o lobo caudado pode cercar completamente a veia cava inferior e pode entrar em contato com o segmento VII no lado direito; um componente retrocaval significativo pode impedir uma abordagem pelo lado esquerdo das veias caudadas. Em transplante hepático com doador vivo (LDLT), durante a hepatectomia direita, a veia caudada deve ser ligada e dividida no lado direito para laçar a veia porta direita. Da mesma forma, o ligamento hepatocaval deve ser dividido para obter exposição à veia hepática direita (RHV). Ao dividir o ligamento hepatocaval, deve-se ter cuidado para ligar e dividir a veia caudada que drena na veia cava inferior neste ligamento.
DIFERENÇA ENTRE ANATOMIA MACROSCÓPICA e MORFOFUNCIONAL
Com base na aparência externa, o fígado tradicionalmente é dividido em quatro lobos: direito, esquerdo, quadrado e caudado. Os lobos direito e esquerdo são separados pelos ligamentos falciformes na superfície ântero-superior do fígado. O ligamento redondo e a fissura para o ligamento de Arantius dividem os lobos na superfície visceral do fígado . No entanto, oculto sob esta aparência externa está a anatomia interna detalhada do fígado, que é relevante tanto cirurgicamente quanto fisiologicamente, também conhecida como a anatomia funcional do fígado.
O plano de divisão entre os lobos direito e esquerdo do fígado não passa pelo ligamento falciforme óbvio, mas sim por um plano que atravessa o leito da vesícula biliar e o entalhe da veia cava inferior, sem outras indicações superficiais. Esta observação foi primeiramente relatada por Rex em 1888 e subsequentemente confirmada por Cantlie em 1897 e por Bradley em 1909. No entanto, foi necessário meio século para que esse conceito fosse amplamente aceito. Este plano imaginário que divide o fígado em metades funcionalmente direita e esquerda é conhecido popularmente como linha de Cantlie (ou plano principal, fissura mediana, linha de Rex).
Com base no suprimento arterial e venoso portal, drenagem venosa hepática e drenagem biliar, o fígado é dividido em lobos funcionais, setores (seções) e segmentos. Embora existam várias nomenclaturas, o conceito de segmentação hepática de Couinaud (1954) é o mais conhecido e amplamente aceito. A arquitetura interna do fígado é composta por uma série de segmentos que se combinam para formar setores separados por fissuras que contêm as veias hepáticas. Basicamente, as três principais veias hepáticas (direita, média e esquerda) dentro das fissuras dividem o fígado em quatro setores, cada um dos quais recebe um pedículo portal. A fissura portal principal contém a veia hepática média e avança desde o meio do leito da vesícula biliar anteriormente até a esquerda da veia cava posteriormente.
O fígado direito e esquerdo, demarcados pela fissura portal principal, são independentes em termos de vascularização portal e arterial e drenagem biliar. A fissura portal direita separa o fígado direito em dois setores: anteromedial (anterior) e posterolateral (posterior). A veia hepática direita corre dentro da fissura direita. Os setores são ainda divididos em segmentos pelos ramos das veias porta. O setor anterior direito é composto pelos segmentos de Couinaud V e VIII. O setor posterior direito é composto pelos segmentos de Couinaud VI e VII. A fissura portal esquerda divide o fígado esquerdo em dois setores, mas não está dentro da fissura umbilical porque esta fissura não é uma fissura portal; em vez disso, ela contém um pedículo portal. A fissura portal esquerda está localizada posteriormente ao ligamento redondo e dentro do fígado esquerdo, ao longo do curso da veia hepática esquerda.
LOBO CAUDADO | SEGMENTO 1
O lobo caudado, ou segmento I, é a porção dorsal do fígado localizada entre a bifurcação da veia porta e a veia cava inferior. O lobo caudado é dividido em porções direita e esquerda, além de um processo caudado. Ele está intimamente relacionado com estruturas vasculares importantes. À esquerda, o lobo caudado fica entre a veia cava inferior posteriormente, o tríade portal esquerdo inferiormente, e a veia cava inferior, veia hepática média e veia hepática esquerda superiormente. O lobo caudado (segmento I) está situado principalmente no lado esquerdo. Ele é suprido por vasos sanguíneos e drenado por tributários biliares tanto do tríade portal direito quanto do esquerdo. A porção direita do lobo caudado recebe predominantemente sangue venoso portal da veia porta direita ou da bifurcação da veia porta principal, enquanto no lado esquerdo, o suprimento portal surge quase exclusivamente do ramo esquerdo da veia porta. O número de ramos portais para o segmento I varia de 1 a 6 (média de 3). O dreno venoso hepático do lobo caudado é único, pois é o único segmento hepático que drena diretamente na veia cava inferior.
DRENAGEM VENOSA
As veias hepáticas desempenham um papel crucial ao drenar o suprimento sanguíneo do fígado para a veia cava inferior. Existem três veias hepáticas principais: veia hepática direita (RHV), veia hepática média (MHV) e veia hepática esquerda (LHV), além de diversas veias menores que também desembocam na veia cava inferior.
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Veia Hepática Direita (RHV):
- A RHV é a maior entre as veias hepáticas e possui um curso curto fora do fígado (aproximadamente 1-2 cm) antes de drenar diretamente na veia cava supra-hepática. Ela se localiza na fissura direita, dividindo o lobo direito em setores posterior (segmentos VI e VII) e anterior (segmentos V e VIII). Principalmente, drena o setor posterior direito e parte do setor anterior direito.
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Veia Hepática Média (MHV):
- A MHV percorre a fissura hepática principal, separando o setor anterior direito (segmentos V e VIII) do lobo quadrado (segmento IV). Ela drena tanto o setor anterior direito quanto o segmento IV. O padrão de ramificação da MHV é crucial em transplantes hepáticos, influenciando o planejamento cirúrgico para escolha adequada de enxertos hepáticos.
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Veia Hepática Esquerda (LHV):
- A LHV está localizada na fissura esquerda ou fissura segmentar esquerda, geralmente próxima ou à direita do ligamento falciforme. Ela drena o segmento lateral esquerdo do fígado (segmentos II e III). Em cerca de 60% das pessoas, a LHV e a MHV se unem para formar um canal venoso único antes de entrar na veia cava inferior abaixo do diafragma. Em outros casos, elas podem drenar separadamente na veia cava inferior.
- Veias Acessórias
- Uma ou mais veias hepáticas acessórias inferiores direitas são a variação mais comum no sistema venoso hepático. Elas estão presentes em 48-55% da população e drenam principalmente o setor posterior direito (segmentos VI e VII) diretamente para a veia cava inferior (IVC). O tamanho das veias hepáticas acessórias direitas (RIHVs) está relacionado ao tamanho da veia hepática direita; ou seja, quanto maior o diâmetro da veia hepática direita, menor o diâmetro da RIHV, e vice-versa. As RIHVs são classificadas em superior, medial e inferior de acordo com sua posição ao entrar na veia cava inferior. A veia hepática acessória superior direita drena principalmente a parte superior do segmento VII, enquanto a veia hepática acessória medial drena a parte média do segmento VII. RIHVs com diâmetro superior a 5 mm devem ser reconstruídas para evitar a congestão do setor posterior direito em transplantes hepáticos de doador vivo (RL LDLT). Pode haver mais de uma RIHV em um indivíduo, e durante a hepatectomia direita, essas veias devem ser dissecadas e ligadas para evitar hemorragias. As Veias Frênicas Inferiores direita e esquerda drenam na parte mais cranial da veia hepática direita e no tronco comum da veia hepática média e veia hepática esquerda, respectivamente. Essas veias frênicas inferiores devem ser ligadas e divididas para obter melhor exposição dessas principais veias hepáticas. Suas extremidades devem ser ligadas quando a veia cava inferior supra-hepática está sendo preparada em um enxerto hepático de doador falecido antes do implante.
HILO HEPÁTICO
Um conhecimento preciso da anatomia hilar e suas variações é fundamental para a dissecação do portal e a divisão das estruturas hilar. Essas etapas são de vital importância no transplante hepático de doador vivo (LDLT). O hilo hepático e o ligamento hepatoduodenal são compostos por três estruturas principais posicionadas em camadas anteroposteriores.
- A veia porta está localizada na parte mais dorsal.
- A artéria hepática fica anterior à veia porta, na camada do meio e medial.
- O ducto biliar está localizado na parte mais ventral e lateral.
Essa organização em camadas facilita a abordagem cirúrgica durante o transplante hepático, permitindo uma dissecção precisa e segura das estruturas do hilo hepático.
VEIA PORTA
A veia porta tem aproximadamente 7-10 cm de comprimento e um diâmetro entre 0,8 e 1,4 cm, sem válvulas. É formada pela confluência da veia mesentérica superior e da veia esplênica atrás do colo do pâncreas. Existem veias pancreaticoduodenais anterior, posterior, superior e inferior que drenam para a veia porta e a veia mesentérica superior (VMS). A veia gástrica esquerda e a veia mesentérica inferior geralmente drenam para a veia esplênica, mas podem drenar diretamente para a veia porta, enquanto os diversos pequenos tributários esplênicos drenam diretamente para a veia esplênica. No porta-hepatis, a veia porta se bifurca em ramos direito e esquerdo antes de entrar no fígado.
O ramo direito da veia porta está localizado anterior ao processo caudado e é mais curto que o ramo esquerdo da veia porta. Próximo à sua origem, ele emite de 1 a 3 ramos para o lobo caudado. A veia porta direita se divide em ramos anterior (que irriga os segmentos V e VIII) e posterior (que irriga os segmentos VI e VII). Cada ramo segmentar se divide ainda em ramos subsegmentares inferior e superior para seus respectivos subsegmentos parenquimatosos.
A veia porta esquerda pode ser dividida em porções transversal e umbilical, delimitadas pelo ligamento venoso, e tem um curso principalmente extra-hepático. Ela começa no porta-hepatis como a parte transversal, que emite um ramo caudado, e segue para a esquerda. No nível da fissura umbilical, a parte umbilical faz uma curva acentuada e segue anteriormente na direção do ligamento redondo, terminando em um fundo de saco próximo à borda inferior do fígado. Mais adiante, a veia porta esquerda se divide em ramos segmentares medial e lateral, cada um com ramos subsegmentares superior e inferior. Variações na veia porta (PV) são comuns (incidência de até 22%) em enxertos de fígado direito-esquerdo (RL) e geralmente estão associadas a altas taxas de variações biliares anatômicas. As implicações clínicas das variações da veia porta e biliares incluem operações tecnicamente desafiadoras com reconstruções complexas, bem como a rejeição de potenciais doadores.
ARTÉRIA HEPÁTICA
A descrição clássica da irrigação arterial do fígado e do sistema biliar é encontrada em apenas cerca de 55% dos pacientes. Artérias hepáticas aberrantes são uma variação comum na anatomia vascular hepática e podem ser classificadas como acessórias (além do suprimento arterial normal) ou substituídas (representando o suprimento arterial primário para o lobo). As incidências de artérias hepáticas aberrantes à esquerda e à direita são de 12-22% e 13-25%, respectivamente. O tronco celíaco se divide em três ramos arteriais principais: artéria gástrica esquerda, artéria esplênica e artéria hepática comum imediatamente após sua origem da aorta. A artéria hepática comum geralmente se origina do tronco celíaco (86%), mas pode ter origem em outras fontes como a artéria mesentérica superior (2,9%), a aorta (1,1%) e, muito raramente, na artéria gástrica esquerda.
A artéria hepática comum então segue horizontalmente ao longo da borda superior da cabeça do pâncreas coberta pelo peritônio da parede posterior da bolsa omental. A artéria gastroduodenal, que irriga o duodeno proximal e o pâncreas, é tipicamente o primeiro ramo da artéria hepática comum. A artéria gástrica direita se origina pouco depois e continua dentro do omento menor ao longo da curvatura menor do estômago. A artéria hepática comum continua como artéria hepática própria, que logo se divide em artérias hepáticas direita e esquerda.
Ao atravessar o ligamento hepatoduodenal, a artéria hepática própria, o ducto biliar comum e a veia porta são envolvidos em uma bainha peritoneal dentro do ligamento hepatoduodenal. A artéria hepática própria bifurca mais cedo do que o ducto biliar comum e a veia porta. Em 80% dos casos, a artéria hepática direita passa posteriormente ao ducto hepático comum antes de entrar no parênquima hepático. Em 20% dos casos, a artéria hepática direita pode estar anterior ao ducto hepático comum. Antes de entrar no fígado, a artéria hepática direita emite a artéria cística no triângulo hepato-cístico, localizado entre o ducto cístico e o ducto hepático comum. Ao alcançar o parênquima hepático, a artéria hepática direita se ramifica em ramos setoriais anterior direito (segmentos V e VIII) e posterior direito (segmentos VI e VII). Uma artéria para o lobo caudado também se origina da artéria hepática direita e irriga o processo caudado e o lado direito do lobo caudado. Essas artérias são encontradas sob os respectivos ramos do ducto biliar. No caso de artéria hepática direita substituída ou acessória da artéria mesentérica superior, a artéria hepática passa posterior e então lateral à veia porta enquanto ascende e fica posterolateral ao ducto colédoco no ligamento hepatoduodenal, onde é suscetível a lesões operatórias se não for reconhecida. A artéria hepática esquerda corre verticalmente em direção à fissura umbilical, onde emite um pequeno ramo (freqüentemente chamado de artéria hepática média ou artéria do segmento 4) para o segmento IV, antes de continuar a irrigar os segmentos II e III. Em 25-30% dos casos, a artéria hepática esquerda surge da artéria gástrica esquerda. Em 40% dos indivíduos, a artéria hepática esquerda se divide em uma artéria segmentar mediana e lateral, cada uma com ramos subsegmentares superior e inferior. Ramos adicionais menores da artéria hepática esquerda irrigam o lobo caudado (segmento I), embora ramos arteriais para o lobo caudado também possam surgir da artéria hepática direita.
A identificação cuidadosa de múltiplas artérias hepáticas e sua fonte, bem como sua preservação, é essencial na coleta de enxertos hepáticos de doadores falecidos. As múltiplas artérias podem ser originadas de um único tronco da artéria celíaca ou da artéria mesentérica superior, anastomosando os ramos separados na bancada. Alternativamente, duas anastomoses separadas podem ser realizadas no receptor. Restaurar o suprimento arterial completo tanto para enxertos parciais quanto completos é vital no transplante hepático para evitar necrose parenquimatosa e complicações biliares.
Os canalículos biliares são formados pela membrana das células parenquimatosas adjacentes e são isolados do espaço perissinusal pelas junções. A bile flui dos canalículos através dos ductúlos (canais de Hering) para os ductos biliares interlobulares encontrados nos pedículos porta.
Ducto Hepático Direito: O ducto hepático direito tem um curso extra-hepático curto formado pela união dos ductos setoriais direito anterior e direito posterior. O ducto setorial posterior direito é formado pela confluência dos ductos dos segmentos VI e VII e tem um curso quase horizontal. O ducto setorial anterior direito é formado pela confluência dos ductos que drenam os segmentos V e VIII. O ducto hepático direito se une ao ducto hepático esquerdo para constituir a confluência hepática, que fica na frente da veia porta direita e forma o ducto hepático comum.
Ducto Hepático Esquerdo: O ducto hepático esquerdo drena os três segmentos – II, III e IV – que constituem o fígado esquerdo. O segmento III é unido por um tributário do segmento IVb para formar o ducto esquerdo, que é similarmente unido pelo ducto do segmento II e do segmento IVa. O ducto hepático esquerdo atravessa sob o fígado esquerdo na base do segmento IV, logo acima e atrás da veia porta esquerda; ele cruza a borda anterior dessa veia e se une ao ducto hepático direito para constituir a confluência dos ductos hepáticos.
Anatomia Biliar Extra-Hepática: Os ductos biliares extra-hepáticos representam os segmentos extra-hepáticos dos ductos hepáticos direito e esquerdo, que se unem para formar a confluência biliar, o ducto hepático comum (CHD) e o ducto biliar comum (CBD). O ducto cístico se une ao CHD para formar o CBD (diâmetro médio de 6 mm), que drena para o duodeno. A confluência dos ductos hepáticos direito e esquerdo ocorre à direita da fissura hilar do fígado, anterior à bifurcação venosa portal e sobrepondo-se à origem do ramo direito da veia porta. A confluência biliar é separada da face posterior do segmento IVB do fígado pela placa hilar, que é a fusão do tecido conjuntivo que envolve os elementos biliares e vasculares com a cápsula de Glisson.
Anomalias dos Ductos Biliares: A confluência biliar normal formada pela união dos ductos hepáticos direito e esquerdo é relatada em apenas 72% dos pacientes. Existem várias variações importantes a serem reconhecidas durante a colecistectomia e a hepatectomia do doador. A Classificação de Huang das variações na anatomia biliar hilar é útil para prever o número de orifícios de ducto biliar do enxerto na aquisição de enxerto do lobo direito em LDLT. Reconhecer essa anatomia biliar é crucial em LDLT para garantir a segurança do doador e resultados biliares ideais no receptor. Essas informações são essenciais para cirurgiões que realizam transplantes de fígado, garantindo uma abordagem precisa e segura durante a remoção do fígado do doador e a anastomose no receptor.
VASCULARIZAÇÃO DA VIA BILIAR
O ducto biliar pode ser dividido em três segmentos com base no seu suprimento sanguíneo: hilar, supraduodenal e retropancreático. Compreender esses segmentos é crucial para procedimentos cirúrgicos, especialmente em transplantes de fígado.
Ducto Supraduodenal:
- O ducto supraduodenal recebe principalmente suprimento sanguíneo arterial que corre axialmente ao longo de suas bordas laterais nas posições de 3 horas e 9 horas.
- A maioria dos vasos arteriais que abastecem o ducto supraduodenal origina-se da artéria pancreaticoduodenal superior, artéria hepática direita, artéria cística, artéria gastroduodenal e artéria retroduodenal.
- Em média, cerca de oito pequenas artérias fornecem suprimento ao ducto supraduodenal.
- 60% dessas artérias têm origem nos principais vasos inferiores e correm para cima, enquanto 38% vêm da artéria hepática direita e de outros vasos, correndo para baixo.
- Apenas 2% do suprimento arterial é não axial, originando-se diretamente do tronco principal da artéria hepática ao lado do canal biliar principal.
Ductos Hilares:
- Os ductos hilares recebem um rico suprimento arterial de vasos circundantes, formando uma rede em sua superfície no plano sub-Glissoniano sob o revestimento hilário.
- Durante a hepatectomia de doador vivo, é crucial colher o ducto hepático do enxerto junto com seu revestimento hilário de Glisson (HPGS) para evitar estenose biliar.
CBD Retropancreático:
- O ducto biliar comum (CBD) retropancreático recebe seu suprimento sanguíneo da artéria retroduodenal, que fornece múltiplos pequenos vasos que formam um plexo mural ao redor do ducto.
Considerações Cirúrgicas:
- Para evitar a isquemia do ducto biliar durante a colheita de um enxerto de lobo direito no transplante de fígado, a artéria hepática direita (RHA) deve ser dividida à direita do ducto biliar se estiver aderida ao CBD. Durante a hepatectomia do receptor, a RHA não deve ser separada do ducto biliar, e se necessário para a reconstrução arterial do enxerto, deve ser dividida à esquerda do ducto biliar. Deve-se ter cuidado para não expor o CBD ao separar a artéria dele.
Drenagem Venosa:
- As veias que drenam os ductos biliares correspondem às artérias descritas, drenando em veias nas posições de 3 horas e 9 horas ao longo das bordas do canal biliar comum. As veias da vesícula biliar não drenam diretamente na veia porta, mas sim neste sistema venoso associado à árvore biliar, indicando uma via venosa portal separada para a bile.
Compreender esses detalhes anatômicos é essencial para cirurgiões que realizam procedimentos complexos no fígado, garantindo cuidado meticuloso para preservar o suprimento sanguíneo e prevenir complicações como estenose ou isquemia biliar.
A vesícula biliar é um reservatório localizado na superfície inferior do lobo direito do fígado (segmentos V e IVB) dentro da fossa cística. Ela é separada do parênquima hepático pela placa cística, composta por tecido conjuntivo que se estende para a esquerda como a placa hilar.
Anatomia da Vesícula Biliar:
- Fundo, Corpo e Istmo: A vesícula biliar é dividida em fundo, corpo e istmo. O fundo geralmente alcança a borda livre do fígado e está intimamente ligado à placa cística.
- Istmo e Bolsa de Hartmann: O istmo ou infundíbulo da vesícula forma um ângulo com o fundo, criando a bolsa de Hartmann, que pode obscurecer o ducto hepático comum e representar um ponto de perigo durante a colecistectomia.
- Ducto Cístico: O ducto cístico surge do infundíbulo da vesícula biliar e se estende para se juntar ao ducto hepático comum.
- Tem um diâmetro de aproximadamente 1-3 mm e seu comprimento varia dependendo do tipo de união com o ducto hepático comum. A mucosa do ducto cístico tem dobras espirais conhecidas como válvulas de Heister. Em 80% dos casos, o ducto cístico se junta à parte supraduodenal do ducto hepático comum, podendo estender-se para áreas retroduodenais ou retropancreáticas. Ocasionalmente, pode se unir ao ducto hepático direito ou a um ducto seccional direito.
Triângulo de Calot:
- Limites:
- Borda superior: superfície inferior do lobo direito do fígado.
- Borda inferior: ducto cístico.
- Base: ducto hepático comum.
- Conteúdo: Artéria cística ou artéria hepática direita.
- A dissecção cuidadosa do triângulo de Calot é crucial durante a colecistectomia para evitar lesões na artéria hepática direita. Em casos de artéria hepática comum ou direita substituída ou acessória, geralmente ela passa por trás do ducto cístico para entrar no triângulo de Calot.
Compreender essa anatomia é essencial para procedimentos cirúrgicos envolvendo a vesícula biliar, garantindo técnicas precisas e seguras para evitar complicações durante a cirurgia e permitir a utilização adequada em transplantes de fígado.
Pringle Maneuver

After the first major hepatic resection, a left hepatic resection, carried out in 1888 by Carl Langenbuch, it took another 20 years before the first right hepatectomy was described by Walter Wendel in 1911. Three years before, in 1908, Hogarth Pringle provided the first description of a technique of vascular control, the portal triad clamping, nowadays known as the Pringle maneuver. Liver surgery has progressed rapidly since then. Modern surgical concepts and techniques, together with advances in anesthesiological care, intensive care medicine, perioperative imaging, and interventional radiology, together with multimodal oncological concepts, have resulted in fundamental changes. Perioperative outcome has improved significantly, and even major hepatic resections can be performed with morbidity and mortality rates of less than 45% and 4% respectively in highvolume liver surgery centers. Many liver surgeries performed routinely in specialized centers today were considered to be high-risk or nonresectable by most surgeons less than 1–2 decades ago.Interestingly, operative blood loss remains the most important predictor of postoperative morbidity and mortality, and therefore vascular control remains one of the most important aspects in liver surgery.
“Bleeding control is achieved by vascular control and optimized and careful parenchymal transection during liver surgery, and these two concepts are cross-linked.”
First described by Pringle in 1908, it has proven effective in decreasing haemorrhage during the resection of the liver tissue. It is frequently used, and it consists in temporarily occluding the hepatic artery and the portal vein, thus limiting the flow of blood into the liver, although this also results in an increased venous pressure in the mesenteric territory. Hemodynamic repercussion during the PM is rare because it only diminishes the venous return in 15% of cases. The cardiovascular system slightly increases the systemic vascular resistance as a compensatory response, thereby limiting the drop in the arterial pressure. Through the administration of crystalloids, it is possible to maintain hemodynamic stability.

In the 1990s, the PM was used continuously for 45 min and even up to an hour because the depth of the potential damage that could occur due to hepatic ischemia was not yet known. During the PM, the lack of oxygen affects all liver cells, especially Kupffer cells which represent the largest fixed macrophage mass. When these cells are deprived of oxygen, they are an endless source of production of the tumour necrosis factor (TNF) and interleukins 1, 6, 8 and 10. IL 6 has been described as the cytokine that best correlates to postoperative complications. In order to mitigate the effects of continuous PM, intermittent clamping of the portal pedicle has been developed. This consists of occluding the pedicle for 15 min, removing the clamps for 5 min, and then starting the manoeuvre again. This intermittent passage of the hepatic tissue through ischemia and reperfusion shows the development of hepatic tolerance to the lack of oxygen with decreased cell damage. Greater ischemic tolerance to this intermittent manoeuvre increases the total time it can be used.
Recurrence after Repair of Incisional Hernia

The incidence of recurrence in incisional hernia prosthetic surgery is markedly lower than in direct plasties. Indeed after the autoplasties of the preprosthetic period, the recurrence rate ranged from 35% for ventral hernias. Chevrel and Flament, in 1990, reported on 1,033 patients who had undergone laparotomy. The recurrence rate at 10-year follow-up was 14–24% for patients treated without the use of prostheses but only 8.6% for those in whom a prosthesis was implanted. A similar incidence was reported by Chevrel in 1995: 18.3% recurrence without prostheses, 5.5% with prostheses. Likewise, Wantz, in 1991, noted a recurrence rate of 0–18.5% in prosthetic laparo-alloplasties.
At the European Hernia Society (EHS)-GREPA meeting in 1986, the recurrence rate without prostheses was reported to be between 7.2 and 17% whereas in patients who had been treated with a prosthesis the recurrence was between 1 and 5.8%. A case study published by Flament in 1999 showed a 5.6% recurrence rate for operations with prostheses placed behind the muscles and in front of the fascia, and a 3.6% of such figure consisted of a small-sized lateroprosthetic recurrence. These rates were in contrast to the 26.8% recurrence reported by other surgeons for operations without prostheses.
Studies of recurrence are, of course, influenced by the size of the initial defect and the length of follow-up. Nevertheless, it is beyond dispute that the use of prostheses is associated with a lower rate of recurrence independent of the nature of the incisional hernia. The factors that lead to relapse are recognisable in the original features of the ventral hernia, i.e. combined musculo-aponeurotic parietal involvement, septic complications in the first operation, the nature and appropriateness of treatment, the kind of prosthesis and its position. Also important is whether the surgery was an emergency case and the relation to occlusive phenomena, visceral damage
and whether these problems were addressed at the same time.
Obesity is also an important risk factor for recurrence. In addition to its association with a higher surgical complications rate, related to the high intraabdominal pressure, there are deficits in wound cicatrisation as well as respiratory and metabolic pathologies. In such patients, the laparoscopic approach is very useful to significantly reduce the onset of general and wall complications, and the data concerning recurrence are encouraging, ranging between 1 and 9% in the largest laparoscopic case studies. The important multicentric study of Heniford et al., in 2000, reported a recurrence rate of 3.4% after 23 months. In 2003, the same author, in a study with an average follow-up of 20 months (range 1–96) showed a recurrence rate of 4.7% for different, identifiable causes: intestinal iatrogenic injuries and mesh infection with its removal, insufficient fixation of the prosthesis and abdominal trauma in the first postoperative period.
The incidence of recurrence after laparoscopic treatment may also be related to general patient factors and to the onset of local complications, mistakes in opting for laparoscopic treatment and deficits in implanting and fixing the prosthesis. With respect to the latter, it is very important to allow a large overlap compared to the diameter of the defect. Long-term data analysis, with large case studies, is still needed to obtain detailed information about recurrence, and this is particularly true in the assessment of relatively new techniques.
Management of gallbladder cancer

Gallbladder cancer is uncommon disease, although it is not rare. Indeed, gallbladder cancer is the fifth most common gastrointestinal cancer and the most common biliary tract cancer in the United States. The incidence is 1.2 per 100,000 persons per year. It has historically been considered as an incu-rable malignancy with a dismal prognosis due to its propensity for early in-vasion to liver and dissemination to lymph nodes and peritoneal surfaces. Patients with gallbladder cancer usually present in one of three ways: (1) advanced unresectable cancer; (2) detection of suspicious lesion preoperatively and resectable after staging work-up; (3) incidental finding of cancer during or after cholecystectomy for benign disease.
SURGICAL MANAGEMENT
Although, many studies have suggested improved survival in patients with early gallbladder cancer with radical surgery including en bloc resection of gallbladder fossa and regional lymphadenectomy, its role for those with advanced gallbladder cancer remains controversial. First, patients with more advanced disease often require more extensive resections than early stage tumors, and operative morbidity and mortality rates are higher. Second, the long-term outcomes after resection, in general, tend to be poorer; long-term survival after radical surgery has been reported only for patients with limited local and lymph node spread. Therefore, the indication of radical surgery should be limited to well-selected patients based on thorough preoperative and intra-operative staging and the extent of surgery should be determined based on the area of tumor involvement.
Surgical resection is warranted only for those who with locoregional disease without distant spread. Because of the limited sensitivity of current imaging modalities to detect metastatic lesions of gallbladder cancer, staging laparoscopy prior to proceeding to laparotomy is very useful to assess the
abdomen for evidence of discontinuous liver disease or peritoneal metastasis and to avoid unnecessary laparotomy. Weber et al. reported that 48% of patients with potentially resectable gallbladder cancer on preoperative imaging work-up were spared laparotomy by discovering unresectable disease by laparoscopy. Laparoscopic cholecystectomy should be avoided when a preoperative cancer is suspected because of the risk of violation of the plane between tumor and liver and the risk of port site seeding.
The goal of resection should always be complete extirpation with microscopic negative margins. Tumors beyond T2 are not cured by simple cholecystectomy and as with most of early gallbladder cancer, hepatic resection is always required. The extent of liver resection required depends upon whether involvement of major hepatic vessels, varies from segmental resection of segments IVb and V, at minimum to formal right hemihepatectomy or even right trisectionectomy. The right portal pedicle is at particular risk for advanced tumor located at the neck of gallbladder, and when such involvement is suspected, right hepatectomy is required. Bile duct resection and reconstruction is also required if tumor involved in bile duct. However, bile duct resection is associated with increased perioperative morbidity and it should be performed only if it is necessary to clear tumor; bile duct resection does not necessarily increase the lymph node yield.
Hepatic Surgery: Portal Vein Embolization

INTRODUCTION
Portal vein Embolizations (PVE) is commonly used in the patients requiring extensive liver resection but have insufficient Future Liver Remanescent (FLR) volume on preoperative testing. The procedure involves occluding portal venous flow to the side of the liver with the lesion thereby redirecting portal flow to the contralateral side, in an attempt to cause hypertrophy and increase the volume of the FLR prior to hepatectomy.
PVE was first described by Kinoshita and later reported by Makuuchi as a technique to facilitate hepatic resection of hilar cholangiocarcinoma. The technique is now widely used by surgeons all over the world to optimize FLR volume before major liver resections.
PHYSIOPATHOLOGY
PVE works because the extrahepatic factors that induce liver hypertrophy are carried primarily by the portal vein and not the hepatic artery. The increase in FLR size seen after PVE is due to both clonal expansion and cellular hypertrophy, and the extent of post-embolization liver growth is generally proportional to the degree of portal flow diversion. The mechanism of liver regeneration after PVE is a complex phenomenon and is not fully understood. Although the exact trigger of liver regeneration remains unknown, several studies have identified periportal inflammation in the embolized liver as an important predictor of liver regeneration.

THECNICAL ASPECTS
PVE is technically feasible in 99% of the patients with low risk of complications. Studies have shown the FLR to increase by a median of 40–62% after a median of 34–37 days after PVE, and 72.2–80% of the patients are able to undergo resection as planned. It is generally indicated for patients being considered for right or extended right hepatectomy in the setting of a relatively small FLR. It is rarely required before extended left hepatectomy or left trisectionectomy, since the right posterior section (segments 6 and 7) comprises about 30% of total liver volume.
PVE is usually performed through percutaneous transhepatic access to the portal venous system, but there is considerable variability in technique between centers. The access route can be ipsilateral (portal access at the same side being resected) with retrograde embolization or contralateral (portal access through FLR) with antegrade embolization. The type of approach selected depends on a number of factors including operator preference, anatomic variability, type of resection planned, extent of embolization, and type of embolic agent used. Many authors prefer ipsilateral approach especially for right-sided tumors as this technique allows easy catheterization of segment 4 branches when they must be embolized and also minimizes the theoretic risk of injuring the FLR vasculature or bile ducts through a contralateral approach and potentially making a patient ineligible for surgery.
However, majority of the studies on contralateral PVE show it to be a safe technique with low complication rate. Di Stefano et al. reported a large series of contralateral PVE in 188 patients and described 12 complications (6.4%) only 6 of which could be related to access route and none precluded liver resection. Site of portal vein access can also change depending on the choice of embolic material selected which can include glue, Gelfoam, n-butyl-cyanoacrylate (NBC), different types and sizes of beads, alcohol, and nitinol plus. All agents have similar efficacy and there are no official recommendations for a particular type of agent.
RESULTS
Proponents of PVE believe that there should be very little or no tumor progression during the 4–6 week wait period for regeneration after PVE. Rapid growth of the FLR can be expected within the first 3–4 weeks after PVE and can continue till 6–8 weeks. Results from multiple studies suggest that 8–30% hypertrophy over 2–6 weeks can be expected with slower rates in cirrhotic patients. Most studies comparing outcomes after major hepatectomy with and without preoperative PVE report superior outcomes with PVE. Farges et al. demonstrated significantly less risk of postoperative complications, duration of intensive care unit, and hospital stay in patients with cirrhosis who underwent right hepatectomy after PVE compared to those who did not have preoperative PVE. The authors also reported no benefit of PVE in patients with a normal liver and FLR >30%. Abulkhir et al. reported results from a meta-analysis of 1088 patients undergoing PVE and showed a markedly lower incidence of Post Hepatectomy Liver Failure (PHLF) and death compared to series reporting outcomes after major hepatectomy in patients who did not undergo PVE. All patients had FLR volume increase, and 85% went on to have liver resection after PVE with a PHLF incidence of 2.5% and a surgical mortality of 0.8%. Several studies looking at the effect of systemic neoadjuvant chemotherapy on the degree of hypertrophy after PVE show no significant impact on liver regeneration and growth.
VOLUMETRIC RESPONSE

The volumetric response to PVE is also a very important factor in understanding the regenerative capacity of a patient’s liver and when used together with FLR volume can help identify patients at risk of poor postsurgical outcome. Ribero et al. demonstrated that the risk of PHLF was significantly higher not only in patients with FLR ≤ 20% but also in patients with normal liver who demonstrated ≤5% of FLR hypertrophy after PVE. The authors concluded that the degree of hypertrophy >10% in patients with severe underlying liver disease and >5% in patients with normal liver predicts a low risk of PHLF and post-resection mortality. Many authors do not routinely offer resection to patients with borderline FLR who demonstrate ≤5% hypertrophy after PVE.
Predicting LIVER REMNANT Function
Careful analysis of outcome based on liver remnant volume stratified by underlying liver disease has led to recommendations regarding the safe limits of resection. The liver remnant to be left after resection is termed the future liver remnant (FLR). For patients with normal underlying liver, complications, extended hospital stay, admission to the intensive care unit, and hepatic insufficiency are rare when the standardized FLR is >20% of the TLV. For patients with tumor-related cholestasis or marked underlying liver disease, a 40% liver remnant is necessary to avoid cholestasis, fluid retention, and liver failure. Among patients who have been treated with preoperative systemic chemotherapy for more than 12 weeks, FLR >30% reduces the rate of postoperative liver insufficiency and subsequent mortality.

When the liver remnant is normal or has only mild disease, the volume of liver remnant can be measured directly and accurately with threedimensional computed tomography (CT) volumetry. However, inaccuracy may arise because the liver to be resected is often diseased, particularly in patients with cirrhosis or biliary obstruction. When multiple or large tumors occupy a large volume of the liver to be resected, subtracting tumor volumes from liver volume further decreases accuracy of CT volumetry. The calculated TLV, which has been derived from the association between body surface area (BSA) and liver size, provides a standard estimate of the TLV. The following formula is used:
TLV (cm3) = –794.41 + 1267.28 × BSA (square meters)
Thus, the standardized FLR (sFLR) volume calculation uses the measured FLR volume from CT volumetry as the numerator and the calculated TLV as the denominator: Standardized FLR (sFLR) = measured FLR volume/TLV Calculating the standardized TLV corrects the actual liver volume to the individual patient’s size and provides an individualized estimate of that patient’s postresection liver function. In the event of an inadequate FLR prior to major hepatectomy, preoperative liver preparation may include portal vein embolization (PVE).
Classroom: Principles of Hepatic Surgery
Videos of Surgical Procedures

This page provides links to prerecorded webcasts of surgical procedures. These are actual operations performed at medical centers in the Brazil. Please note that you cannot send in questions by email, though the webcast may say that you can, because you are not seeing these videos live. The videos open in a second window. If you have a pop-up blocker, you will need to disable it to view the programs.
Videos of Surgical Procedures
Surgical Management of Cholangiocarcinoma

Cholangiocarcinoma (CCA) is a rare but lethal cancer arising from the bile duct epithelium. As a whole, CCA accounts for approximately 3 % of all gastrointestinal cancers. It is an aggressive disease with a high mortality rate. Unfortunately, a significant proportion of patients with CCA present with either unresectable or metastatic disease. In a retrospective review of 225 patients with hilar cholangiocarcinoma, Jarnagin et al. reported that 29 % of patients had either unresectable disease were unfit for surgery. Curative resection offers the best chance for longterm survival. Whereas palliation with surgical bypass was once the preferred surgical procedure even for resectable disease, aggressive surgical resection is now the standard.
Classroom: Surgical Management of Cholangiocarcinoma
Strangulation in GROIN HERNIAS
Importance
Declining Mortality Rates
In both the UK and the USA, the annual death rate due to inguinal and femoral hernias has significantly decreased over the past two to three decades. In the UK, deaths from these hernias declined by 22% to 55% between 1975 and 1990. Similarly, in the USA, the annual deaths per 100,000 population for patients with hernia and intestinal obstruction decreased from 5.1 in 1968 to 3.0 in 1988. For patients with obstructed inguinal hernias, 88% underwent surgery, with a remarkably low mortality rate of 0.05%. These improvements suggest that elective groin hernia surgery has played a crucial role in reducing overall mortality rates.
Elective Surgery and Strangulation Rates
Supporting this observation, the USA has lower rates of strangulation compared to the UK, possibly due to the threefold higher rate of elective hernia surgeries in the USA. Nevertheless, statistics indicate that the rate of elective hernia surgeries in the USA per 100,000 population decreased from 358 to 220 between 1975 and 1990, although this may be an artifact of data collection rather than a genuine decline.
Mortality Analysis from UK and Denmark Studies
During 1991–1992, the UK National Confidential Enquiry Into Perioperative Deaths investigated 210 deaths following inguinal hernia repair and 120 deaths following femoral hernia repair. This inquiry, which focuses on the quality of surgery, anesthesia, and perioperative care, found that many patients were elderly (45 were aged 80–89 years) and significantly infirm; 24 were ASA grade III and 21 ASA grade IV. The majority of postoperative mortality was attributed to preexisting cardiorespiratory issues.
A nationwide study in Denmark of 158 patients who died after acute groin hernia repair by Kjaergaard et al. also found that these patients were old (median age 83 years) and frail (>80% with significant comorbidity), with frequent delays in diagnosis and treatment. These findings highlight the need for high-quality care by experienced surgeons and anesthetists, especially for patients with high ASA grades.
Postoperative Care Recommendations
Postoperative care for these patients should occur in a high-dependency unit or intensive therapy unit. This might necessitate transferring selected patients to appropriate hospitals and facilities. Decisions about interventional surgery should be made in consultation with the relatives of extremely elderly, frail, or moribund patients, adopting a humane approach that may rule out surgery.
Emergency Admissions and Prioritization
Forty percent of patients with femoral hernias are admitted as emergency cases with strangulation or incarceration, while only 3% of patients with direct inguinal hernias present with strangulation. This disparity has implications for prioritizing patients on waiting lists when these hernias present electively in outpatient clinics.
Risk of Strangulation
A groin hernia is at its greatest risk of strangulation within three months of onset. For inguinal hernias, the cumulative probability of strangulation is 2.8% at three months after presentation, rising to 4.5% after two years. The risk is much higher for femoral hernias, with a 22% probability of strangulation at three months, rising to 45% at 21 months. Right-sided hernias have a higher strangulation rate than left-sided hernias, potentially due to anatomical differences in mesenteric attachment. The decline in hernia-related mortality in both the UK and USA underscores the importance of elective hernia surgery. Ensuring timely surgery, especially for high-risk femoral hernias, and providing high-quality perioperative care for elderly and frail patients are crucial steps in further reducing mortality and improving patient outcomes.
Evidence-Based Medicine
In a randomized trial, evaluating an expectative approach to minimally symptomatic inguinal hernias, Fitzgibbons et al. in the group of patients randomized to watchful waiting found a risk of an acute hernia episode of 1.8 in 1,000 patient years. In another trial, O’Dwyer and colleagues, randomizing patients with painless inguinal hernias to observation or operation, found two acute episodes in 80 patients randomized to observation. In both studies, a large percentage of patients randomized to nonoperative care were eventually operated due to symptoms. Neuhauser, who studied a population in Columbia where elective herniorrhaphy was virtually unobtainable, found an annual rate of strangulation of 0.29% for inguinal hernias.
Management of Strangulation
The diagnosis of hernias is primarily based on clinical symptoms and signs, supplemented by imaging studies when necessary. Pain at the hernia site is a constant symptom. In cases of obstruction with intestinal strangulation, patients may present with colicky abdominal pain, distension, vomiting, and constipation. Physical examination may reveal signs of dehydration, with or without central nervous system depression, especially in elderly patients with uremia, along with abdominal signs of intestinal obstruction.
Femoral hernias can be easily missed, particularly in obese women, making a thorough physical examination essential for an accurate diagnosis. However, physical examination alone is often insufficient to confirm the presence of a strangulated femoral hernia versus lymphadenopathy or a lymph node abscess. In such cases, urgent radiographic studies, such as ultrasound or CT scan, may be necessary.
The choice of incision depends on the type of hernia if the diagnosis is clear. When there is doubt, a half Pfannenstiel incision, 2 cm above the pubic ramus extending laterally, provides adequate access to all types of femoral or inguinal hernias. The fundus of the hernia sac is exposed, and an incision is made to assess the viability of its contents. If nonviability is detected, the transverse incision should be converted into a laparotomy incision, followed by the release of the constricting hernia ring, reduction of the sac’s contents, resection, and reanastomosis. Precautions must be taken to avoid contamination of the general peritoneal cavity by gangrenous bowel or intestinal contents.
In most cases, once the constriction of the hernia ring is released, circulation to the intestine is restored, and viability returns. The intestine that initially appears dusky or non-peristaltic may regain color with a short period of warming with damp packs. If viability is doubtful, resection should be performed. Resection rates are highest for femoral or recurrent inguinal hernias and lowest for simple inguinal hernias. Other organs, such as the bladder or omentum, should be resected as needed.
After peritoneal lavage and formal closure of the laparotomy incision, specific repair of the hernia should be performed. Prosthetic mesh should not be used in a contaminated operative field due to the high risk of wound infection. Hernia repair should follow the general principles of elective hernia repair. It is important to remember that in this predominantly frail and elderly patient group with a high postoperative mortality risk, the primary objective of the operation is to stop the vicious cycle of strangulation, with hernia repair being a secondary objective.
Key Point
The risk of an acute groin hernia episode is of particular relevance, when discussing indication for operation of painless or minimally symptomatic hernias. A sensible approach in groin hernias would be, in accordance with the guidelines from the European Hernia Society to advise a male patient, that the risk of an acute operation, with an easily reducible (“disappears when lying down”) inguinal hernia with little or no symptoms, is low and that the indication for operation in this instance is not absolute, but also inform, that usually the hernia after some time will cause symptoms, eventually leading to an operation. In contrast, female patients with a groin hernia, due to the high frequency of femoral hernias and a relatively high risk of acute hernia episodes, should usually be recommended an operation.
Wound Healing

There are many local and systemic factors that affect wound healing. The physician should be actively working to correct any abnormality that can prevent or slow wound healing.
Local Factors
A health care provider can improve wound healing by controlling local factors. He or she must clean the wound, debride it, and close it appropriately. Avulsion or crush wounds below under general management of wounds) need to be debrided until all nonviable tissue is removed. Grossly contaminated wounds should be cleaned as completely as possible to remove particulate matter (foreign bodies) and should be irrigated copiously. Bleeding must be controlled to prevent hematoma formation, which is an excellent medium for bacterial growth. Hematoma also separates wound edges, preventing the proper contact of tissues that is necessary for healing.
Radiation affects local wound healing by causing vasculitis, which leads to local hypoxia and ischemia. Hypoxia and ischemia impede healing by reducing the amount of nutrients and oxygen that are available at the wound site. Infection decreases the rate of wound healing and detrimentally affects proper granulation tissue formation, decreases oxygen delivery, and depletes the wound of needed nutrients. Care must be taken to clean the wound adequately. All wounds have some degree of contamination, if the body is able to control bacterial proliferation in a wound, that wound will heal. The use of cleansing agents (the simplest is soap and water) can help reduce contamination. A wound that contains the highly virulent streptococci species should not be closed. Physicians should keep in mind the potential for Clostridium tetani in wounds with devitalized tissue and use the proper prophylaxis.
Systemic Factors
In addition to controlling local factors, the physician must address systemic issues that can affect wound healing. Nutrition is an extremely important factor in wound healing. Patients need adequate nutrition to support protein synthesis, collagen formation, and metabolic energy for wound healing. Patients need adequate vitamins and nutrients to facilitate healing; folic acid is critical to the proper formation of collagen. Adequate fat intake is required for the absorption of vitamins D, A, K, and E. Vitamin K is essential for the
carboxylation of glutamate in the synthesis of clotting factors II, VII, IX, and X. Decreasing clotting factors can lead to hematoma formation and altered wound healing. Vitamin A increases the inflammatory response, increases collagen synthesis, and increases the influx of macrophages into a wound. Magnesium is required for protein synthesis, and zinc is a cofactor for RNA and DNA polymerase. Lack of any one of these vitamins or trace elements will adversely affect wound healing. Uncontrolled diabetes mellitus results in uncontrolled hyperglycemia, impairs wound healing, and alters collagen
formation. Hyperglycemia also inhibits fibroblast and endothelial cell proliferation within the wound. Medications will also affect wound healing. For example, steroids blunt the inflammatory response, decrease the available vitamin A in the wound, and alter the deposition and remodeling of collagen. Chronic illness (immune deficiency, cancer, uremia, liver disease, and jaundice) will predispose to infection, protein deficiency, and malnutrition, which, as noted previously, can affect wound healing. Smoking has a systemic effect by decreasing the oxygencarrying capacity of hemoglobin. Smoking may also decrease collagen formation within a wound. Hypoxia results in a decrease in oxygen delivery to a wound and retards healing.
Abdominal Surgical Anatomy

The abdomen is the lower part of the trunk below the diaphragm. Its walls surround a large cavity called the abdominal cavity. The abdominal cavity is much more extensive than what it appears from the outside. It extends upward deep to the costal margin up to the diaphragm and downward within the bony pelvis. Thus, a considerable part of the abdominal cavity is overlapped by the lower part of the thoracic cage above and by the bony pelvis below. The abdominal cavity is subdivided by the plane of the pelvic inlet into a larger upper part, i.e., the abdominal cavity proper, and a smaller lower part, i.e., the pelvic cavity. Clinically the importance of the abdomen is manifold. To the physician, the physical examination of the patient is never complete until he/she thoroughly examines the abdomen. To the surgeon, the abdomen remains an enigma because in number of cases the cause of abdominal pain and nature of abdominal lump remains inconclusive even after all possible investigations. To summarize, many branches of medicine such as general surgery and gastroenterology are all confined to the abdomen.