Current classification of inguinal hernia: time to correct, update and change?

Hehir Dermot J and Mannion Jennifer


Repair of an inguinal hernia is a commonly performed surgical procedure. Current classifications are predominantly attributable to Hesselbach, who in the 19th Century described the anatomy of the inguinal region and the relationship of inguinal hernia to the inferior epigastric vessels. However largely due to the dynamic visualization of inguinal anatomy at video-surgery, our better understanding of inguinal anatomy is facilitated; consequently, we believe that the inferior epigastric vessels have a coincidental anatomical relationship and have no significant causal relationship to groin herniation. Furthermore, we believe the current classification, using the terms ‘direct’ and ‘indirect’ are anatomically incorrect. It is our opinion that such classification should be abandoned in favour of a simplified system which reflects our enhanced appreciation of the anatomy.

Key-words: Inguinal Hernia, Classification


Considering  all  that  is  written  about  the  radical  treatment  of  the  inguinal  hernia  up  until  now,  it  can  be  somewhat  risky  to  try  to  publish  more  about  this  subject “   (Eduardo  Bassini 1890 On the treatment of inguinal hernia)  

It  is  estimated  that  5%  of the  population  will  develop  an  inguinal  hernia  -  the  lifetime  risk  is  27%  in  males  and  3%  in  females [1] .  The  cost  to  society  is  enormous,  since inguinal hernia  surgery  is  the  most  commonly  performed  intermediate surgical   procedure.   In  the  USA  alone,  ¾  million  operations  are  performed  annually [2]. Data  from  large  multi – institution  series  suggest  that  tension  free  mesh  repair  is  now  the  preferred  modality [3];  debate  continues  whether  mesh  placement  via  open  or  minimally  invasive (laparoscopic  or  robotic) techniques  is  optimal.   Proponents  of  each  technique  site  advantages  i.e.  less  pain [4], shorter  hospital  stay,  early  return  to  employment or  disadvantages  such  as  cost,   learning  curve,  visceral  injury [5].


The  inguinal  canal , which  in  reality  is  the  epicentre  of  inguinal  hernia  pathology,  is  an  oblique  area  extending  from  the  deep  to  superficial   inguinal   rings. The  floor  is  formed  by  the  inguinal  ligament  which   extends  between  the  anterior  superior  iliac  spine  laterally  and  the  pubic  tubercle  medially  – it  represents  the  reflected  margin  of  the  external  oblique  aponeurosis.  The  oblique   nature  of  the  canal  is  related  to  the   insertion  of  the  conjoint  tendon, (comprising  fibres from both the internal oblique and the transversus abdominus muscles), onto  the  pectineal  line  of  the  pubis [6].

 The  roof  consists  of  an  arch   formed  by the  transversus   abdominis muscle  and  lower  fibres  of  internal  oblique muscle.    The  anterior  wall  –  as  visualised  at  conventional  open hernia  repair  is  formed  by  the  external  oblique  medially  and  the  internal  oblique  laterally. The  posterior  wall  is  formed  by  the  conjoint  tendon  (fibres  of  internal  oblique /  transversus   abdominis). 

The  internal  oblique  muscle, with  assistance  from  the  transversus   abdominis  (collectively  the  conjoint  tendon)  is  postulated  to  create  a  type  of  protective  mechanism  against  inguinal  hernia  development [7, 8]

The transversalis fascia is a potential bilayered wrapping created from infolding of the embryological umbilical funiculus [9].

Aetiology of Inguinal Hernia

More  than  two  centuries  ago  (prior  to  the  dynamic  videoscopy  era),  Hesselbach  recorded  the  inferior  epigastric vessels  as  the  definitive  anatomical  landmark with  “direct” hernia  medial  to  and  “indirect”   lateral  to  the  vessels [10] . Thus, these  terms  historically  relate to his belief  that  the  herniated  structure  traverses  the  abdominal  wall  either  directly  or  in  an  indirect  oblique  fashion  via  the  inguinal  canal . 

The frequent coexistence  of  inguinal  hernia  in  patients  with  collagen  disorders (10),  suggest  a  defect  in  the  collagen  fibre  mechanism.  Such  pathology  may  explain  the  higher  incidence  of  incisional  hernia  in  aortic  aneurysm  surgery  and  defects  associated  with  Ehlers – Danlos  syndrome [11].  

Historically,  it  was  assumed  that   lateral  “indirect”  hernia  were  due  to  failure  of  obliteration  of  the  embryological  processus  vaginalis in males; a similar process in females involves a delayed or incomplete closure of the canal of Nuck [12].   Approximately 10% of  children  with  observed  asymptomatic   patent  processus  vaginalis  develop an inguinal  hernia,  in  comparison  to  none  of  those  in whom the process is  obliterated [13].  The theory is further supported by adult data - patent  processus  vaginalis  significantly  increases  the  risk  of post-operative  inguinal  hernia  following  robotic  prostatectomy [14]. In contrast however, inguinal hernia  may  develop  after  closure  of  the  processus  vaginalis  suggesting  that  the  condition  is in fact  acquired [15]. Fruchaud   hypothesised  that  groin  hernia  formation  is  due  to  the  adoption  of  upright  posture  in  modern  man [13].   More  recently,   Radoievitch’s  angle  between  the  ipsilateral  inguinal  ligament  and a  line traversing  both  anterior  superior  iliac  spines  has  been  associated  with  inguinal   herniation  due  to  abnormal   pelvic  anatomical  angulation [16].   There  is a  documented  increase in  inguinal  herniation  with  age,  which  may implicate  muscle  sarcopenia [17]. The occurrence of combined hernia (involving the medial inguinal fossa, internal inguinal ring and the supravesical fossa) is a common occurrence particularly in the elderly. These hernias appear to be progressive in nature and histopathological evaluation reveals fatty degeneration of myocytes with surrounding chronic inflammatory infiltrate often extending to involve all components of this area of the abdominal wall and associated structural damage to the inferior epigastric vessels. The author postulates that over time these pathological changes enables the progression to tricomponent herniation until the entire inguinal floor is devastated allowing a single protrusion to emerge [18].


The  internal  oblique  muscle   forms  at  least  a  significant  component  of  three  of  the  four  anatomical ‘walls’  of  the  inguinal  canal. Thus a healthy internal oblique musculature is a major protective mechanism in the prevention of inguinal herniation. Damage to the internal oblique ie age related degeneration or collagen disorder, results in a global weakness in the inguinal region.

The proliferation of video facilitated groin hernia repair has facilitated our understanding of groin anatomy in vivo (Hesselbach did not have this luxury). It is now clearly possible to see internal defects in the inguinal abdominal wall and more importantly to demonstrate the global weakness associated with herniation. 

The ‘direct / indirect’  classifications  - such as Nyhus, Gilbert and Schumpelick are primarily based on anatomical localization of the hernia in conjunction with the size [19]. Other current classifications are based on findings attributable to Hesselbachs theory and therefore may not be appropriate for comparing data from different studies. Critics have argued they lack objectivity and prove difficult to remember leading to inconsistent usage [20].

It is our opinion that the terms ‘direct’ and ‘indirect’ for the description of inguinal hernias should be abandoned. We believe that a rather  less specific description  such as  ‘ a two finger swelling in the medial aspect of the right groin’ may be more appropriate.


The current classification of Inguinal herniation is based on historical anatomical dissection and for two centuries the inferior epigastric vessels have been unquestionably accepted as the distinction between ‘direct’ and ‘indirect’ inguinal herniation. It is our opinion that such classification should now be replaced, as it fails to appreciate our 21st century knowledge of anatomy and the pathological processes involved in inguinal herniation.

Prior publication

Oral Presentation at the 102nd American College of Surgeons Clinical Congress (2016 Washington Seattle)


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