Furthermore xenical 120 mg mastercard, A-V dissociation can be seen with supraventricular rhythms buy xenical 60mg low price, fusion complexes can result from two ventricular ectopic foci safe 120mg xenical, and morphologic and/or axis characteristics established for patients with normal P 120 mg xenical amex. In the absence of pre-excitation a supraventricular impulse must pass through the His bundle and the specialized ventricular conducting system before initiating depolarization of the ventricles. This may result because no engagement of the His–Purkinje system by the ventricular impulse occurs (probably uncommon), or because retrograde His bundle activation occurs during ventricular activation and is obscured by the large ventricular deflection in the His bundle recording. His deflections can usually be observed if attention is given to catheter position. One may identify His bundle activity before ventricular activation (in this instance, the H-V interval is shorter than normal; e. If His bundle deflections are not seen, one must differentiate the absence of retrograde activation of the His– Purkinje P. This can be fortuitously observed if a sinus impulse conducts antegradely to the His bundle producing a clear His deflection. In these instances, linking of the His bundle potential to atrial activation proves that they are due to antegrade depolarization and are unrelated to the tachycardia. Retrograde block in the A-V node is present because atrial activation is dissociated from the tachycardia. It is often difficult to determine whether the recorded His deflection is antegrade or retrograde—or for that matter whether an apparent His bundle deflection is really a right bundle branch potential. Two techniques that may be used to clarify the situation are (a) recording right and left bundle branch potentials to demonstrate that their activation begins before His bundle activation and (b) His bundle pacing producing a longer H-V interval than the one noted during the tachycardia. Both of these are extremely difficult to do but can help define the mechanism of His bundle activation and the tachycardia origin. The simplest methods for verifying proper catheter position include the following: (a) the immediate appearance of His bundle deflections on termination of the tachycardia, or conversely, disappearance of the His bundle deflection on initiation of the tachycardia, without catheter manipulation; (b) spontaneously occurring or induced supraventricular capture of the His–Purkinje system (with or without ventricular capture) during the tachycardia with the sudden appearance of His bundle deflections; and (c) in the presence of supraventricular capture, H-V intervals comparable to those during sinus rhythm (Figs. We have found that the use of more closely spaced bipolar electrodes (l to 5 mm apart) facilitate identification of His bundle activity when it occurs within the ventricular electrogram. The second atrial impulse (A) conducts through the His bundle but fails to alter the tachycardia. The first and third sinus complexes block in the A-V node due to retrograde concealment. Two complexes later, another supraventricular fusion is observed, again without influencing the tachycardia. This demonstrates lack of requirement of the His bundle for perpetuation of the tachycardia. If His deflections are not spontaneously observed during the tachycardia, because of either poor position or obscuration of the His deflection by the ventricular electrogram, rapid atrial pacing can be used to clarify the issue in some cases. Thus, knowledge of A-V conduction during sinus rhythm may be necessary to define what is a “normal” H-V interval during the tachycardia. Some investigators , suggest that the site of origin of such a tachycardia is within the His–Purkinje system. As stated earlier, pre-excited tachycardia using either an A-V or nodoventricular bypass tract must be excluded (see Chapter 10). It is not rare for a tachycardia to have a V-H interval less than the antegrade H-V interval (Fig. Retrograde conduction time over the His–Purkinje system is actually much greater than the “V-H” observed during the tachycardia. Depending on the relative conduction time up the His–Purkinje system and through slowly conducting P. Atrial pacing is begun (arrow) at a cycle length of 480 msec, which is gradually reduced to 400 msec. As the atrial-paced cycle length decreases, a greater degree of ventricular activation is produced via the normal conducting system. The His deflection typically occurs before the right bundle deflection with an H-V interval approximating the H-V interval during sinus rhythm. Theoretically, if there is prolonged retrograde conduction over the His–Purkinje system, producing a markedly delayed His deflection (very long V-H), the “in parallel” activation of the His bundle would appear as a “normal” H-V interval. In this case, one must demonstrate that the His deflection is not a requisite for subsequent ventricular activation and thus is not a reflection of bundle branch reentry. Certain criteria are necessary for the diagnosis of bundle branch reentry, all of which provide P. The mechanisms of bundle branch reentry and its variants are discussed in greater detail later in this chapter. B: The schema shows that propagation of the impulse from the reentrant circuit to the His–Purkinje system is more rapid than that to the remainder of the myocardium, resulting in a short V-H interval. In this instance, conduction to the His–Purkinje was far more rapid than that to the ventricular myocardium, resulting in early His–Purkinje activation. These differences make it mandatory that these arrhythmias not be lumped together in terms of response to stimulation, effects of pharmacologic therapy, effectiveness of ablation, and clinical outcome. Anatomic Substrate The most common anatomic substrate for all these arrhythmias is chronic coronary artery disease, usually associated with prior infarction. Arrhythmias that are due to coronary artery disease are the only ones for which we have a reasonable understanding of the pathophysiologic substrate required for their genesis. Although sustained uniform monomorphic tachycardia may occur in the presence of either hypertrophic or idiopathic dilated cardiomyopathy, or even in patients with normal hearts, it is relatively uncommon. In these instances, the pathophysiologic basis for the arrhythmia is not well understood although patchy or segmental fibrosis is a common denominator. Arrhythmogenic right ventricular dysplasia has similar pathology as infarction, but it starts on the epicardium and additionally has fatty infiltration of the myocardium. This may occur because in most cases there is patchy fibrosis instead of the large areas of contiguous scar seen in infarction. Regardless of the underlying cardiac pathophysiology, sustained monomorphic tachycardia can be studied electrophysiologically such that interpretation of the mechanism and development of therapy is possible. Electrophysiologic studies are most useful in patients with coronary artery disease and prior infarction. The pathologic substrate for patients with ventricular tachyarrhythmias associated with coronary artery disease is 20 21 22 23 usually a prior myocardial infarction resulting in wall motion abnormalities. The second group of patients who present with a cardiac arrest are those who have severe coronary artery disease and relatively normal ventricular function; in this group the arrest is most likely due to acute ischemia. Our patient population is clearly selected so that we study patients with lower ejection fractions, recognizing that lower ejection fraction per se places a person at high risk for sudden death. The extent of infarction, and perhaps location involving the septum, may be the two important prognostic factors associated with these 21 24 malignant sustained ventricular arrhythmias. The cycle lengths of the tachycardias occurring early after infarction, however, tend to be faster, and the tachycardia is more poorly tolerated. This may reflect evolving scar formation, which when ultimately completed, may be related to longer tachycardia cycle lengths, owing to abnormalities of conduction with which it is 26 associated (see following discussion). Thus, some components of the anatomic substrate must be relatively fixed once infarction has 27 occurred. This is supported by inducibility at 10 and 100 days in an Ovine infarction model. Moreover the ability of programmed stimulation to predict risk of sudden cardiac arrest and survival postinfarction lead credence to 28 this hypothesis. Attempts to make these correlations are fraught with selection and/or entry bias, which is inherent in selecting patients from catheterization laboratories, coronary care units, or exercise laboratories. Similarly, patients studied following cardiac arrest are a selected group of survivors, and as such may not reflect the timing from infarction to cardiac arrest of nonsurvivors. However, this may indicate some of the characteristics of those patients likely to survive. Of more than 1,100 selected survivors of cardiac arrest associated with coronary artery disease who we have studied, the highest incidence (≈50%) of cardiac arrest occurred in the first 6 to 12 months following infarction. After the first year following infarction, the incidence of cardiac arrest decreases rapidly, such that within 3 years the incidence is low. In the thrombolytic and primary angioplasty era, the timing of these events has not changed, but, as stated above, their frequency has been significantly reduced. The pathophysiologic substrate in disease states other than coronary artery disease is less clear. Electrophysiologic Substrate The clinically measurable electrophysiologic consequences of infarction that are potentially arrhythmogenic include abnormalities of conduction and refractoriness, heterogeneity of conduction and refractoriness, enhanced automaticity, and areas of inexcitability. Unipolar (top) and bipolar (bottom) signals recorded with the Rhythmia mapping system. The bipolar signal removes the large farfield signal recorded in the two unipolar electrograms from which the bipolar signal is derived. We developed criteria for normal, abnormal, and fractionated electrograms using bipolar signals recorded with a Bard Josephson catheter (see Fig. Normal electrograms had sharp, biphasic, or triphasic spikes with amplitudes of ≥3 mV, durations of ≤70 msec, and/or an amplitude/duration ratio of ≥0. We defined fractionated electrograms as abnormal electrograms that fell outside the 95% confidence limits of amplitude and duration of all abnormal electrograms. The most common abnormalities were low voltage and increase in electrogram duration, both of which appear to be nonspecific markers of infarction or even poor contact. Multicomponent and fractionated electrograms, isolated late potentials and late electrograms were more closely related to 31 arrhythmogenic sites; but the positive predictive value was only ∼30%. Only 14% of “sites of origin” came from sites that demonstrated normal electrograms. It should be obvious that since mapping catheters have different size electrode (tip and ring), normal and abnormal electrogram characteristics need to be defined for each catheter. Subsequent intraoperative studies using a 20 pole plaque electrode showed that successful surgery was associated with elimination of isolated late potentials and split potentials suggesting mechanistic significance 37 (Fig. The first two complexes are sinus in origin and the left ventricular recordings show markedly abnormal electrograms. Multiple components are present, and the electrogram exceeds 160 msec in duration.
A plain X-ray of abdomen showing a large soft tissue swelling displacing the gut supports the diagnosis discount xenical 60 mg without a prescription. Yes discount xenical 60 mg amex, hemihypertrophy is one the predisposing congenital conditions for Wilms’ tumor discount xenical 120 mg fast delivery. Other such conditions are Beckwith syndrome generic xenical 120mg otc, aniridia, duplication of kidney or ureter, hypospadias, undescended testis, and ambiguous genitalia. Exposure Conventionally speaking, the term, immunity, refers to to a microbe second time provokes the adaptive immunity the defense mechanism that protects an individual against to recall previous express and react with a rapid rise in invasion by an infection. Innate immunity may be genetically passed on from Cellular Components one generation to another without depending on previous contact with a microbe. When it indicates a degree of T ymus and bursa of Fabricius (marrow in man) form resistance to all infections, it is termed nonspecifc. Spleen and lymph glands there is a resistance to a particular pathogen, it is called constitute the peripheral lymphoid tissues. Innate immunity is also expressed in relation to response has two stages: species, race or individual. It should be considered primitive with no Phagocytic response consists of destroying the foreign memory. In the conduct of phagocytic response, additional Lymphocytic response is afected by either humoral or factors such as complement and opsonin may be required. If the invading agent is destroyed by phagocytosis, immune Humoral immunity is concerned with synthesis and response stops here only. However, if antigenic products release of antibodies (immunoglobulins) secreted by plas- are produced, the next step, i. Its which is the sheet-anchor of the immunologic system, functional cell is B lymphocyte, the bursa-dependent cell, must follow. T helper cells are essential for Complement refers to a series of factors in the normal their transformation into antigen recognition cells and pro- serum that are activated by antigen-antibody interac- duction of immunoglobulins. T suppressor cells suppress tion and subsequently mediate a number of biologically the activity and lessen formation of antibodies. It forms about 10% of human immune response is maintained within a tolerable level. Tere are 9 distinct components of com- On entry of an ofending agent (antigen), B cells plement system, one of them having 3 subunits (C´1g´, develop into plasma cells which secrete specifc antibodies C´1r´, C´1s´) thereby making a total of 11 proteins. Once the illness is over, level of of event in which complement components react in spe- circulating antibodies falls slowly over a period of several cifc sequence following activation of antigen-antibody weeks. In case the same illness returns, level of antibodies complexes and culminating in immune cytolysis is known against the antigen rises rapidly, thereby halting the as classical C´ pathway. Activation of C´3´ without prior invasion by the same antigen and acquisition of specifc participation of C´1´, C´4´ and C´2´ is called alternate immunity. Activities of the complement immunity against mechanisms by which the antibody was produced earlier. Functions C´1´ and C´4´, C´1´, C´4´, C´2´ and C´3´: Neutraliza- of the B cells include: tion of viruses Protection against Staphylococcus, Streptococcus, Hemo- C´4a´, C´3a´, C´5a´: Capillary dilatation phillus, Pneumococcus C´5a´: Chemotaxis of neutrophils, monocytes, eosino- Neutralization of viruses to prevent initial infection phils Action as a barrier along gastrointestinal and respira- C´3b´: Opsonization, enhancement of cell-mediated cyto- tory tracts toxicity stimulation of production of B cells lymphokines Active lysis of cells of autologus origin or engagement C´3b´, C´3d´: Increased induction of antibody formation in antigen-antibody complex disease C´3c´: Induction of granulocytosis Interference with T killer cells activity, or directly or C´5´: Opsonization of fungi indirectly blocking the reaction. In the thymus hormone, thymosin, is claimed to maintain their fetus, it is by far the only immunoglobulin present. Functions of T lymphocytes include: newborn receives it, by transport across the placenta, T helper function in sufcient amount depending on the gestational age, T suppressor function weight and efciency of placental function. Tere are further z Containment of fungal infections (candida) subclasses of IgG, say IgG1, IgG2, IgG3 and IgG4, based on diferences in heavy polypeptide chain (Fc). Te exact role of IgM in z Rejection of allograft (tumors) immune response is not yet clearly understood. Te major soluble factors include: z Transient hypogammaglobulinemia G Mitogenic factor which enhances lymphocyte multipli- z Panhypogammaglobulinemia (congenital agammaglobulinemia, cation Bruton disease) Permeability increasing factor z Dysgammaglobulinemia (common varied immunodefciency) Lymphocytotoxin Selective IgA defciency Selective secretory IgA defciency Migration inhibiting factor which favors phagocytosis Selective IgM defciency Transfer factor which transfers to the uncommitted IgG subgroup defciency. T cell (cellular) defects Cellular immune response ends up in destruction of the z Congenital thymic hypoplasia (DiGeorge syndrome) antigen. Tis may either be directly through the action of the z Nezelof syndrome sensitized lymphocytes or by activity of lymphocytotoxins. By immunodefciency is meant that one or more defense Neutrophil defects mechanisms are impaired or lacking. It may be primary z Qualitative when there is no obvious systemic disease to explain its oc- Chronic granulomatous disease Chediak-Higashi syndrome currence. In the secondary type, the cause is clearly outside Job syndrome the lymphoid system, e. Primary defciency is far less Cyclic neutropenia than the secondary defciency (Fig. Both sexes are afected, the incidence being z Ataxia telangiectasia, characterized by hereditary cerebellar higher in preterm infants. Te condition is associated ataxia and conjunctival telangiectasia together with frequent with frequent bacterial infections in which situation the sinopulmonary infections infant needs to be administered 0. Clinical manifestations include repeated infections with Pneumococcus, staphylococcus and Hemophilus infuenza as also viruses, especially echotype 30, skin disorders like eczema and recurrent abscesses, malabsorption, Lam- blia giardia infestation, disaccharide intolerance and increased incidence of malignancy. Diagnosis is made by assaying the serum immunoglobulin IgM and IgA nearly absent and IgG invariably less than 200 mg/dL. Long-term complications include bronchiectasis, rheumatoid arthritis, malignancy, hemo- lytic anemia and infection with Pneumocystis carinii. Dysgammaglobulinemia (common varied immuno- defciency) refers to states of absence or defciency of one or more immunoglobulins. There was demonstrable defciency in T cell system with normal serum globulin is a remarkable association with autoimmune disease like levels. Te patient, how- Features (fne, thin hair, short-limbed dwarfsm with ever, has normal capacity to synthesize IgG and IgM antibod- characteristic roentgenographic features) of cartilage- ies. Overall is scaling erythroderma and total alopecia (absence of incidence varies between 1 in 400 and 1 in 1,000. Selective defciency of secretory IgA may occur in two Graft-vs-host disease after blood transfusion. Inselective IgM defciency, prominent clinical features include fulminant hematogenous spread of bacterial Congenital thymic hypoplasia or aplasia (DiGeorge infections, atopy and splenomegaly. Common associates syndrome) is characterized by embryonic combined def- are Whipple disease, regional enteritis and lymphoid ciency of thymus and parathyroids (both arise from third nodular hyperplasia. A vigorous antibiotic treatment as and fourth pharyngeal pouches) in association with con- soon as infection is suspected is indicated. Clinical symptoms suggestive of combined B and T cell Chronic mucocutaneous candidiasis. This 10-year-old boy that showed waxing and waning from early infancy, this 1-year-old had presented with chronic generalized lymphadenopathy (most marked in recurrent epistaxis and purpura, discharging ears and frequent intercur- the cervical and axillary regions where the nodes showed multiple dis- rent infections. Level of lgM was remarkably low though IgA prominence as also widening of the superior mediastinum (not due to and lgG levels were elevated. Emperically, antituberculous therapy was given Features of all above, except chronic mucocutaneous without any relief. Cellular and candidiasis and nodular lymphoid hyperplasia antibody responses were found to be normal. Mild Te bactericidal defect seems to be due to change in dysfunction of T cell occurs. Response to corticosteroids is frequently develop malignant reticuloendotheliosis. It occurs and IgE deficiency and variable degree of T cell de- exclusively in males. Death usually fol- Many patients have depressed chemotaxis of neutro- lows development of malignant lymphoma. Infection occurs usually by Lazy leucocyte syndrome, a specifc disorder of leuco- bacteria which are normally of low virulence and fungi. Te kopenia and absence of polymorphonuclear motility defect can be detected in vitro by the nitroblue tetrazolium from bone marrow into circulation. Normally, almost 90% of leucocytes reduce Congenital chronic neutropenia, isoimmune neonatal the dye to a purple-black compound. In granulomatous neutropenia, cyclic neutropenia, Shwachmann-Diamond disease, hardly 10% or even less are able to do so. Te syndrome and congenital splenic defects fgure among the disease is usually X-linked recessive (males afected, prominent quantitative defciency states of neutrophils. Absence of C´1 may cause hereditary angioneurotic z Severe tricuspid regurgitation. Hypercatabolism z lmmunosuppressive therapy z Severe/fulminant infection of C´3 causes increased frequency of infections and that of z Cytotoxic therapy z Congenital rubella C´5 causes recurrent pyogenic infections. Te child with immunodefciency invariably tics of infections such are: shows growth retardation with short stature, irritability Prolonged duration with complications Repeated infections with hardly any symptom free period and pallor. Pyoderma, eczema, stomatitis, perianal exco- Multisystem involvement riation and ear discharge are common accompaniments. Investigations z Family history of a severe infection, early deaths of members, collagenosis or consanguinity may provide a clue to an inherited Initial/screening tests immunodefciency defect. Peculiar faces (micrognathia, DiGeorge syndrome Specifc tests hypertelorism, low-set ears, (congenital thymic hypoplasia) z lmmunoglobulin levels: IgA, IgG and IgM are done notched pinna) initially and, if warranted, IgD and IgE may be done Albinism Chediak-Higashi disease at a later stage. Conjunctivitis IgA defciency z Opsonin function: The function of opsonins (the Uveitis IgA defciency two chief ones are antibodies and complements) is Telangiectasia Ataxia telangiectasia tested by mixing white blood cells and bacteria in the presence of subject’s serum. It is examined for the number of bacteria Chronic ear discharge Chronic granulomatous disease, X- which have been engulfed by the cells. A count linked lymphoproliferative disease, of less than 300 bacteria/100 white cells suggests Wiskott-Aldrich syndrome, opsonic abnormal opsonic function. Dextocardia Immotile cilia syndrome A good history, clinical examination and the screening Hepatosplenomegaly Chronic granulomatous disease tests mentioned here are capable of identifying about a large majority of the immunodefciency states in pediatric Ataxia Ataxia telangiectasia practice. Arthritis Complement defciency Treatment Poor muscle mass with joint IgA defciency enlargement It is outlined in discussion of specifc entities in appropriate chapters. A breakdown in the mecha- nism of recognition of self-antigen and nonself-antigen Extensive warts T cell defect may lead to development of autoantibodies in a group of Candidiasis T cell defect disorders referred to as autoimmune diseases.
One is an open surgical the Pneumo technique using a Hasson trocar; the other is a closed technique using a Veress needle xenical 60mg on line. The author personally uses the closed technique with a Veress needle buy cheap xenical 60mg, and in more than 20 years of advanced laparoscopy per- forming several thousand procedures order 120mg xenical overnight delivery, the author has experienced only one injury (on a distended stomach on his third laparoscopic case in 1989) order xenical 120mg on line. When a Veress needle is used, the author recommends that a nasogastric tube be inserted into the stomach and the stomach defated so as to avoid puncture. When per- forming lower abdominal surgery it is also important to insert a urinary catheter. The skin around the incision is grasped with one hand and lifted up, and the Veress needle is then slowly inserted. Care is needed to make sure that the red line of the Veress needle (when using a disposable version) appears during fascial penetration; a sudden disappearance of the red line is accompanied by a noise that will indicate that the needle is in the abdomen. If the needle is not in the virtual abdominal space but is in a fatty intraabdominal deposit, the red line will move up and down indi- cating incorrect placement of the needle. In all cases a confrmatory test should be per- formed using saline or preferably an empty syringe. An empty 10 cm3 syringe fxed on the needle is frst aspirated to make sure that there is no intraabdominal fuid coming from the needle – such as blood, bowel content, or bile. Ten cubic centimeter of air is then injected into the peritoneal cavity; if it cannot be aspirated back the injected air must have diffused into the cavity and the needle is properly placed. If the injected air comes back into the syringe the needle is not in the peritoneal cavity, and so it should be pushed a little further. A low gas fow (or no fow) with high pressure indicates that the needle is not in the abdomen. It is advisable to change the position of the needle using the same skin incision but in another direction. It is also possible to change from the umbilical site to the left upper quadrant (Palmer’s point). After three failed attempts, the general rule is that one should convert to an open laparoscopy procedure using a Hasson trocar. The Hassan open trocar is inserted under direct vision and the ties secured to the trocar. Direct closed laparoscopy with the insertion of a trocar without pneumoperitoneum (not to be confused with gasless laparoscopy where no trocars are used at all), as advocated by some gynecologists, is dangerous and should never be used under any circumstances. Troubleshooting Loss of Pneumoperitoneum Occasionally during a laparoscopic case, the surgeon may feel that there is no working space. The knowledge and interpretation of the indicators on the insuffation unit will determine the origin of the problem and how to address it. Pressure higher than 15 mmHg (a) Patient is not fully paralyzed or is waking up during the surgery (b) Pressure is set higher than 15 mmHg (c) The trocar valve is closed or there is a kink in the tube 2. The suction is working and is stronger than the insuffator Control of Bleeding of Unnamed Vessels Principles of An unnamed vessel can be controlled in the same manner as a main vessel (see below), Hemostasis but usually simple compression with an atraumatic clamp and careful electrocautery will control the bleeding, so long as the major abdominal organs are kept under vision at an appropriate distance. Compression is one of the best possible means of achieving hemostasis on a rough surface. This compression follows the principles of open surgery, namely temporary hemostasis allowing cleaning of the area and identifcation of the nature of the bleeding. It is critical to keep the bleeding space dry while applying the electrical surgical current by suctioning constantly as the electrical current is applied. Control of Bleeding of a Main Named Vessel There is a major difference between handling a hemorrhage from a main vessel and that from an unnamed vessel. A main vessel requires vascular compression, retraction of the camera to protect the lens from splashing blood, and irrigation of the feld. The surgeon should never attempt to clip a main vessel blindly in a bloody operating site, as visceral injuries will occur. For bleeding originating from a main abdominal vessel, compression cannot be applied using 2 × 2 gauze. Instead it is necessary to use a large atraumatic clamp such as a small-bowel clamp or long Kelly with atraumatic jaws and tips that will compress the bleeding structure and its surrounding structures (Fig. Gentle and atraumatic application will avoid injuring or rupturing the vessel itself. The same procedure as above is then followed: cleaning, aspiration, irrigation, and application of clips, electrical current, or a suture, depending on the situation. A vessel should not be divided before its proximal and distal ends are identifed and the vessel has been controlled without incorporating adjacent structures in the clips. The use of monopolar current carries the risk of intraabdominal diffusion and transmission of power to adjacent structures. During application of monopolar current other organs should not be touched and the tip of the electrocautery instrument should be kept under direct vision at all times. This is especially true when using monopolar current in con- junction with scissors with long blades or long noninsulated instruments. The risk of intraabdominal explosion is more theoretical than real and has not occurred in the author’s practice, but the use of nitrous oxide in this setting is not recommended because it supports combustion. Bipolar instruments are probably safer but have the disadvantage of producing more smoke and are slower to achieve hemostasis. Of the available bipolar instruments, bipolar scissors and bipolar grasping forceps are the most useful and should be available in advanced laparoscopic trays. Harmonic shears can also be used on most of the unnamed vessels, up to a diameter of 5 mm, above which it is safer to apply clips or ties. Ideally such a device should deliver appro- Suction Devices priate irrigation at variable fow rates, with the possibility of hydrodissection if required. The suction component of irrigation systems is its Achilles heel because the suction pipe is usually connected to the central facility on the operating room wall. Suction is therefore too strong and will simply suck away the pneumoperitoneum, immediately obscuring the view before achieving a result. As a result the suction force has to be made adjustable, usually using small forceps, especially when suction is immediately needed (as for hemorrhage). The tip of the suction cannula is usually sharp and can traumatize tissues or vessels. The handpiece containing the valve has to be small, and is held ergonomically in the palm of the hand with separate trumpets for suction and irrigation. Finally, many devices offer the possibility of insertion of standard laparoscopic instruments through a large (10 mm) shaft but the complexity of the mounting has pre- vented its generalized adoption. J Am Coll Surg 181(6):565–566 Curtis P, Bournas N, Magos A (1995) Simple equipment to facilitate operative laparoscopic surgery (or how to avoid a spaghetti junction). Surgery 146(2):381–386 Frangov T, Mladenov V, Mouiel J, Katkhouda N (1994) Diagnostic laparoscopy and lapa- roscopic surgery, their development and outlook. Arch Surg 140(1):80–84 Meyers W, Katkhouda N (1999) Handoscopic surgery: a prospective multi-center trial of a minimally invasive technique for complex abdominal surgery. Surg Endosc 8(9):1129–1130 Unger S, Olsen D, Nagy A, Zucker K, Katkhouda N (1994) Laparoscopic surgery: surgical education, The People Republic of China. World J Surg 17:3–7 a b Cholecystectomy 2 Basic The patient is placed in the supine position with either the left arm or both arms Laparoscopic tucked. The surgeon stands on the left and the assistant stands on the right side of the Cholecys patient. The camera assistant stands on the left side of the patient to the left of the sur- tectomy geon, or alternatively the assistant may hold the camera from the other side of the table (on the right side of the patient) if there is no dedicated camera assistant. After insertion of the umbilical trocar for the laparoscope, the remaining trocars should be introduced taking into account the patient’s body habitus. A standardized routine may be used for trocar insertion, but should be adapted based on patient size. For example if patient is obese, the trocars should be placed closer to the costal margin (Fig. After the abdomen is insuffated, the patient is positioned in reverse Trendelenburg and right side up. This ensures that the duodenum and transverse colon are moved down by gravity and improves exposure. The next trocar to be inserted is the lateral trocar used to retract the fundus and inspect the triangle of Calot. Quite often this trocar is inserted too low so that the grasper cannot reach the liver, and thus is unable to fip the gallbladder together with the liver to ensure proper exposure. For this reason it is recommended that the frst 5 mm trocar be inserted just under the right costal margin and as laterally as possible. Before insertion it is also necessary to ensure that the handle of the grasper is not blocked by the patient’s fank or knees. Pushing the abdominal wall with the left hand will indent the abdomen and help ideal placement of the trocars by visualization of the entry site. It is usually inserted to the right of the falciform ligament, just at the level of the border of the right lobe of the liver. A subxyphoid trocar for instrument; B midcla- vicular port for left hand of surgeon; D grasper for retraction of gallbladder; E additional stan- dard port for obese. If this trocar is too low, however, the angle of dissection will be incorrect and there will be confict with the laparoscope (“knitting needle” effect). Once the operating port has been inserted, the fundus of the gallbladder is retracted and an additional 5 mm trocar is inserted for lateral retraction of Hartmann’s pouch. The operating port, the video laparoscope, and the lateral trocar are triangulated to avoid a “knitting needle” effect between the graspers and the video laparoscope (Fig.