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By N. Riordian. University of Massachusetts at Amherst.

The head of the patient’s bed should be raised not more than 30 degrees cheap cialis black erectile dysfunction caused by radical prostatectomy, neuromuscular blockage should be administrated [75] 800 mg cialis black mastercard erectile dysfunction what to do, and relief of pain and anxiety with proper medication should be initiated promptly [52] purchase cialis black australia cialis causes erectile dysfunction. Prokinetic agents such as erythromycin and metoclopramide may help in avoiding paralytic ileus [77] cheap cialis black 800 mg with amex erectile dysfunction 19 year old male. Administration of loop diuretics to enhance fuid removal may be of ben- eft if patients’ hemodynamic allow its administration. Removal of fuid by extracor- poreal techniques is more effective and may have an immediate effect [78]. Seven patients responded to nonoperative therapy, but the remaining 13 patients had progressive deterioration of organ dysfunction and received interventional decompressive procedure. The effects of abdominal decompression on organ functions were summarized in a collective review of 250 patients who underwent midline laparotomy [83, 85]. Decompression had a positive effect on hemodynamic, respiratory, and renal func- tion parameters. However, despite initial improvement almost in all patients, mortality rate of 50% was recorded. In another retrospective study, the mortality after various techniques of decompression was 46% [83]. Different surgical techniques exist but currently there are no randomized trials comparing the outcomes of the different surgical approaches. Acute arterial occlusion is the most common cause of mesenteric ischemia and results from embolic occlusion in 40–50% and thrombotic occlusion in 20–35% of the patients [87]. This policy includes a routine re-exploration of the abdomen 24–48 h after the index operation carried out in an effort to preserve as much bowel as possible. Some surgeons select aggressive approach with a scheduled second-look proce- dure in any patient who undergoes bowel resection and primary anastomosis [88, 89], whereas others suggest a more selective approach [90, 91]. Other researchers found that fewer than half the patients underwent a second- look operation and more than 40% benefted from the procedure that resulted appro- priate treatment. In mesenteric venous thrombosis, the thrombotic process extends well beyond what appears to be the compromised bowel. Therefore, a second-look exploration is often the only way to establish the full extent of nonviable bowel. In a nonrandomized case–control study [92], patients undergoing planned relap- arotomy were matched with patients who underwent relaparotomy on demand. There was no signifcant difference in mortality between the groups, but multiple organ failure and septic complications were more common in the patients who underwent planned relaparotomy. Second-look laparotomy may be avoided if the experienced surgeon identifes clear margins of demarcation between well-vascularized and necrotic bowel in a hemodynamically stable patient. Until large prospective studies are available, the indications for a second- look operation should be evaluated with caution and be based on surgeon experi- ence and based on the surgical fndings as well as patient hemodynamics. The strategy of leaving many patients with open abdomen was frst reported from the Mayo Clinic. Although many surgeons practice this approach in diverse abdominal pathologies, no common denominator can be outlined in the reported cohort. Only well-conducted studies based on internationally agreed nomenclature will address the issue of who will be the patient that will beneft from the open abdomen and damage control strategy. Packing and planned reexploration for hepatic and retroper- itoneal hemorrhage: critical refnements of a useful technique. Management strategies for the open abdomen sur- gery of the American Association for the surgery of trauma membership. Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus defnitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Indications for use of damage control surgery and damage control interventions in civil- ian trauma patients: a scoping review. Coccolini F, Biff W, Catena F, Ceresoli M, Chiara O, Cimbanassi S, Fattori L, Leppaniemi A, Manfredi R, Montori G, Pesenti G, Sugrue M, Ansaloni L. Three indications for the “open abdomen”, anatomical, logistical and physiological: how are they different? The management of the open abdomen in trauma and emergency general surgery: part 1-damage control. Systematic review and meta-analysis of the open abdomen and temporary abdominal closure techniques in non-trauma patients. Anatomical, physiological, and logistical indications for the open abdomen: a proposal for a new classifcation system. The open peritoneal cavity: etiology correlates with the likelihood of fascial closure. The open abdomen and temporary abdominal closure systems–historical evolution and systematic review. Temporary closure of the open abdomen: a systematic review on delayed primary fascial closure in patients with an open abdomen. Long-term vacuum-assisted closure in open abdomen due to secondary peritonitis: a retrospective evaluation of a selected group of patients. Multicentre prospective study of fascial clo- sure rate after open abdomen with vacuum and mesh-mediated fascial traction. Factors affecting primary fascial closure of the open abdomen in the nontrauma patient. Vacuum and mesh-mediated fascial trac- tion for primary closure of the open abdomen in critically ill surgical patients. Prospective evalua- tion of vacuum-assisted closure in abdominal compartment syndrome and severe abdominal sepsis. Deferred primary anastomosis versus diversion in patients with severe secondary peritonitis managed with staged laparotomies. Abdominal com- partment syndrome and intra-abdominal sepsis: two of the same kind? Supranormal trauma resuscitation causes more cases of abdominal compartment syndrome. Secondary abdominal compartment syndrome: an underappreciated manifestation of severe hemorrhagic shock. Is the evolving management of intra-abdominal hypertension and abdominal compartment syndrome improving survival? A decision rule to aid selection of patients with abdominal sepsis requiring a relaparotomy. Open versus closed management of the abdo- men in the surgical treatment of severe secondary peritonitis: a randomized clinical trial. Comparison of on-demand vs planned relaparot- omy strategy in patients with severe peritonitis: a randomized trial. Topical negative pressure in managing severe peritonitis: a positive contribution? Initial experience of laparostomy with immediate vacuum therapy in patients with severe peritonitis. Peritoneal negative pressure therapy prevents multiple organ injury in a chronic porcine sepsis and ischemia/reperfusion model. Planned relaparotomy vs relaparotomy on demand in the treatment of intra-abdominal infections. Mortality and morbidity of planned relaparot- omy versus relaparotomy on demand for secondary peritonitis. Costs of relaparotomy on-demand versus planned relaparotomy in patients with severe peritonitis: an economic evaluation within a randomized controlled trial. Complications of planned relaparotomy in patients with severe general peritonitis. Open management of the abdomen and planned reoperations in severe bacterial peritonitis. Results from the international conference of experts on intra-abdominal hypertension and abdominal compartment syndrome, I: defni- tions. Prevalence of intra-abdominal hyperten- sion in critically ill patients: a multicentre epidemiological study. Incidence and clinical effects of intra-abdominal hypertension in critically ill patients. Treatment of abdominal compartment syn- drome with subcutaneous anterior abdominal fasciotomy in severe acute pancreatitis. Transverse laparostomy is feasible and effective in the treatment of abdominal compartment syndrome in severe acute pancreati- tis. Surgical management of intra-abdominal hypertension and abdominal compartment syndrome. Results from the international confer- ence of experts on intra-abdominal hypertension and abdominal compartment syndrome. Prevention of abdominal compartment syndrome by absorbable mesh prosthesis closure. Intra-abdominal hypertension after life-threatening penetrating abdominal trauma: prophylaxis, incidence, and clinical relevance to gastric mucosal pH and abdominal compartment syndrome. Classifcation of acute pancreatitise2012: revision of the Atlanta classifcation and defnitions by interna- tional consensus. Abdominal compartment syndrome in patients with severe acute pancreatitis in early stage. Clinical relevance of intra-abdominal hypertension in patients with severe acute pancreatitis. Results from the international confer- ence of experts on intra-abdominal hypertension and abdominal compartment syndrome. Early recognition of abdominal compart- ment syndrome in patients with acute pancreatitis.

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A frequently encountered problem is that the duration of sampling is not long enough to define accurately the elimination phase purchase cialis black online from canada impotence pills for men. Conversely discount 800mg cialis black with mastercard erectile dysfunction natural remedies diabetes, samples are sometimes obtained too infrequently following drug administration to be able to characterize the distribution phases accurately generic 800 mg cialis black amex erectile dysfunction hiv medications. In fact buy cialis black us impotence versus erectile dysfunction, some drugs have two-compartment10 kinetics in some patients and three-compartment kinetics in others. In selecting a pharmacokinetic model, the most important factor is that it accurately characterizes the measured concentrations. In general, the model with the smallest number of compartments or exponents that accurately reflects the data is used. However, it is good to consider that the data collected in a particular study may not be reflective of the clinical pharmacologic issues of concern in another situation, making published pharmacokinetic model parameters potentially irrelevant. In this case, the pharmacokinetic models will not be of use in designing dosing regimens for drug X that avoid toxic drug concentrations at 1 minute. With this technique, pharmacokinetic parameters were estimated independently for each subject and then averaged to provide estimates of the typical parameters for the population. One problem with this approach is that if outliers are present, averaging parameters could result in a model that does not accurately predict typical drug concentrations. Currently, most pharmacokinetic models are developed using population pharmacokinetic modeling, which has been made feasible because of advances in modeling software and increased computing power. With these techniques, the pharmacokinetic parameters are estimated using all the concentration versus time data from the entire group of subjects in a single stage, using sophisticated nonlinear regression methods. This modeling technique provides single estimates of the typical parameter values for the population. Noncompartmental (Stochastic) Pharmacokinetic Models Often investigators performing pharmacokinetic analyses of drugs want to avoid the experimental requirements of a physiologic model—data or empirical estimations of individual organ inflow and outflow concentration profiles and organ tissue drug concentrations are required in order to identify 680 the components of the model. Although compartmental models do not40 assume any physiologic or anatomic basis for the model structure, investigators often attribute anatomic and physiologic function to these empiric models. Even if the disciplined clinical pharmacologist avoids41 overinterpretation of the meaning of compartment models, the simple fact that several competing models can provide equally good descriptions of the mathematical data, or that some subjects in a data set may better fit with a three-compartment model rather than the two-compartment model that provides the best fit for the other data set subjects, leads many to question whether there is a true best model architecture for any given drug. Therefore, some investigators choose to employ mathematical techniques to characterize a pharmacokinetic data set that attempt to avoid any preconceived notion of structure, and yet yield the pharmacokinetic parameters that summarize drug distribution and elimination. These techniques are classified as noncompartmental techniques or stochastic techniques and are similar to the methods based on moment analysis utilized in process analysis of chemical engineering systems. Although these techniques are often called model- independent, like any mathematical construct, assumptions must be made to simplify the mathematics. The basic assumptions of noncompartmental analysis are that all of the elimination clearance occurs directly from the plasma, the distribution and elimination of drug is a linear and first-order process, and the pharmacokinetics of the system does not vary over the time of the data collection (time-invariant). All of these assumptions are also made in the basic compartmental, and most physiologic, models. Therefore, the main advantage of the noncompartmental pharmacokinetic methods is that a general description of drug absorption, distribution, and elimination can be made without resorting to more complex mathematical modeling techniques. In fact, when properly defined, the estimates of these parameters from the noncompartmental approach and a well-defined compartmental model yield similar values. However, the premise behind developing models to better characterize and understand the effects of various physiologic and pathologic states on drug distribution and elimination was that the relationship between a dose of drug and its effect(s) had already been characterized. As computational power and drug assay technology grew, it became possible to characterize the relationship between a drug concentration and the associated pharmacologic effect. As a result, pharmacodynamic studies since the nineties have focused on the quantitative analysis of the relationship between the drug concentration in the blood and the resultant effects of the drug on physiologic processes. Drug–Receptor Interactions Most pharmacologic agents produce their physiologic effects by binding to a drug specific receptor, which brings about a change in cellular function. The majority of pharmacologic receptors are cell membrane bound proteins, although some receptors are located in the cytoplasm or the nucleoplasm of the cell. Binding of drugs to receptors, like the binding of drugs to plasma proteins, is usually reversible, and follows the Law of Mass Action: This relationship demonstrates that the higher the concentration of free drug or unoccupied receptor, the greater the tendency to form the drug– receptor complex. Plotting the percentage of receptors occupied by a drug against the logarithm of the concentration of the drug yields a sigmoid curve, as shown in Figure 11-9. In the left panel, the response data is plotted against the dose data on a linear scale. In the right panel, the same response data are plotted against the dose data on a logarithmic scale yielding a sigmoid dose–response curve that is linear between 20% and 80% of the maximal effect. The percentage of receptors occupied by a drug is not equivalent to the percentage of maximal effect produced by the drug. In fact, most receptor systems have more receptors than required to obtain the maximum drug effect. The presence of “extra” unoccupied receptors will promote the45 formation of the drug–receptor complex (Law of Mass Action, Equation 11- 17); therefore, near-maximal drug effects can occur at very low drug concentrations. This not only allows extremely efficient responses to drugs, but it provides a large margin of safety—an extremely large number of a drug’s receptors must be bound to an antagonist before the drug is unable to produce its pharmacologic effect. For example, at the neuromuscular junction, only 20% to 25% of the postjunctional nicotinic cholinergic receptors need to bind acetylcholine to produce contraction of all the fibers in the muscle, while 75% of the receptors must be blocked by a nondepolarizing neuromuscular antagonist to produce a significant drop in muscle strength. There are two primary schemes by which the binding of an agonist to a receptor changes cellular function: receptor-linked membrane ion channels called ionophores, and guanine nucleotide binding proteins, referred to as G-proteins. The nicotinic cholinergic receptor in the neuromuscular postsynaptic membrane is one example of a receptor–ionophore complex. Binding of acetylcholine opens the cation ionophore, leading to an influx of Na ions,+ propagation of an action potential, and, ultimately, muscle contraction. Desensitization and Downregulation of Receptors Receptors are not static entities. Prolonged exposure of a receptor to its agonist leads to desensitization—subsequent doses of the agonist will produce lower maximal effects. With sustained elevation of the cytosolic second messengers downstream of the G-proteins, pathways to prevent further G-protein signaling are activated. Phosphorylation by G- protein receptor kinases and arrestin-mediated blockage of the coupling site needed to form the active heterotrimeric G protein complex prevents G protein coupled receptors from becoming active. Arrestins and other cell membrane proteins can tag receptors that have sustained activity, so that these non–G-protein receptors are internalized and sequestered so they are no longer accessible to agonists. Similar mechanisms will prevent the trafficking of stored receptors to the cell membrane. The combined increased rate of internalization and decreased rate of replenishing of receptor results in downregulation—a decrease in the total number of receptors. Signals that produce downregulation with sustained receptor activation are essentially reversed in the face of constant receptor inactivity. Therefore, chronically denervated neuromuscular junctions, just like cardiac tissue constantly bathed with adrenergic antagonists, will upregulate the specific receptors in an attempt to produce a signal in the face of lower concentrations of agonists. Agonists, Partial Agonists, and Antagonists Drugs that bind to receptors and produce an effect are called agonists. Different drugs that act on the same receptor may be capable of producing the same maximal effect (Emax), although they may differ in the concentration that produces the effect (i. Agonists that differ in potency but bind to the same receptors will have parallel concentration–response curves (Fig. Differences in potency of agonists reflect differences in affinity for the receptor. Partial agonists are drugs that are not capable of producing the maximal effect, even at very high concentrations (Fig. Compounds that bind to receptors without producing any changes in cellular function are referred to as antagonists— antagonists make it 684 impossible for agonists to bind their receptors. Competitive antagonists bind reversibly to receptors, and their blocking effect can be overcome by high concentrations of an agonist (i. Therefore, competitive antagonists produce a parallel shift in the dose–response curve, but the maximum effect is not altered (Fig. This has the same effect as reducing the number of receptors and shifts the dose–response curve downward and to the right, decreasing both the slope and the maximum effect (Fig. The effect of noncompetitive antagonists is reversed only by synthesis of new receptor molecules. Figure 11-10 Schematic pharmacodynamic curves, with dose or concentration on the x- axis and effect or receptor occupancy on the y-axis, that illustrate agonism, partial agonism, and antagonism. Drug A produces a maximum effect, Emax, and a 50% of maximal effect at dose or concentration E50,A. Drug B, a full agonist, can produce the maximum effect, Emax; however, it is less potent (E50,B > E50,A). Drug C, a partial agonist, can only produce a maximum effect of approximately 50% Emax. If a competitive antagonist is given to a patient, the dose response for the agonist would shift from curve A to curve B—although the receptors would have the same affinity for the agonist, the presence of the competitor would necessitate an increase in agonist in order to produce an effect. In fact, the agonist would still be able to produce a maximal effect, if a sufficient overdose was given to displace the competitive antagonist. However, the competitive antagonist would not change the binding characteristics of the receptor for the agonist and so curve B is simply shifted to the right but remains parallel to curve A. In contrast, if a noncompetitive antagonist binds to the receptor, the agonist would no longer be able to produce a maximal effect, no matter how much of an overdose is administered (curve C). Partial agonists may produce a qualitatively different change in the receptor, whereas antagonists bind without producing a change in the receptor that results in altered cellular function. The underlying mechanisms by which different compounds that bind to the same receptor act as agonists, partial agonists, or antagonists are not fully understood. Dose–Response Relationships Dose–response studies determine the relationship between increasing doses of a drug and the ensuing changes in pharmacologic effects.

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The average size of the orbit: the depth of the adult orbit ranges from 4 to 5 cm; width at the entrance is about 4 cm and the height is typically less than 3 discount cialis black 800mg online impotence tumblr. They separate the eye sockets from the rest of the skull: the upper wall of the orbit goes from the anterior cranial fossa and the frontal sinus; the lower wall of the orbit proceeds from the maxillary sinuses; the medial wall of the orbit runs from the nasal cavity and the lateral wall proceeds from the temporal fossa buy cialis black 800mg on line erectile dysfunction young adults treatment. Fissura orbitalis superior (located in posterior regio) connects orbit with fossa cranii superior discount 800mg cialis black visa erectile dysfunction causes high blood pressure. Fissure orbitalis inferior between lateral and inferior walls connects orbit with temporal and infratemporal fossae purchase cialis black master card erectile dysfunction medication with high blood pressure, sphenoid sinus. Eyelids are plates made of skin and cartilages that are curved according to the shape of forward eye segment. This layer is composed of the eyelid cartilages and the orbital septum attached to them. The posterior surface of the cartilage century and orbital septum is lined with mucous membranes - the conjunctiva, or conjunctiva palpebrarum, which goes on into the sclera of the eyeball, conjunctiva bulbi. Places where conjunctiva transits from eyelids to sclra form the upper and lower conjunctiva’s domes - fornix conjunctivae superior et inferior. For the inspection of the upper conjunctiva’s dome it is necessary to turn the upper eyelid out. The frontal edge of the eyelids has eyelashes, which have sebaceous glands at their basements. It is possible to see the holes of specific sebaceous, or meibomian, glands landed in the thickness of the eyelid cartilage closer to the rear edge of the eyelids. The movable edges of the eyelids of the medial and lateral angles of the eyes form angles that are fixed to the bones of the eye socket with tendons. It is located in the cavity of the eye socket, even though holding it only partially. Eyeball is surrounded by fascia, eyeball vagina, or vagina bulbi, or Tenon’s capsule. Tenon’s capsule, which covers the eyeball almost across its entire length, except for the region corresponding to the cornea (in the front) and the place of passage of the optic nerve (in the rear), suspends the eyeball in the orbit among the fat cellular tissue, while being fixed with the fascial strands that go to the wall of the eyesocket and its edges. Tenon’s capsule doesn’t stick tightly with the eyeball: there is always a small fissure, spatium episclerale, which allows the eyeball to move easily. Muscular apparatus of eyesockets includes 6 extraocular muscles (4 rectus muscles and 2 oblique muscles) and the muscle that lifts the upper eyelid (m. It has the following boundries: sclera limits it from the front; optic canal orbital aperture limits it from behind. The upper boundary of the nasal region is the horizontal line connecting the medial ends of the eyebrows (the root of the nose), the lower boundary is the line drawn through the attachment of the nasal septum and the lateral boundaries of the nasal area are defined by the nasobuccal and nasolabial folds. External nose, nasus externus, is formed with the nasal bones at the top, while at the sides it is formed with the frontal process of the maxilla and cartilages. At the lower point lateral cartilage joins on each side with the larger ala nasi cartilage. At the same time it is attached to the lower end of the nasal bone and the frontal bone of the upper jaw from behind. Greater ala nasi cartilage is paired and is located below the corresponding lateral cartilage of the nose, limiting entrance to the nasal cavity. Sometimes you can find additional cartilage of variable sizes between the lateral cartilage and a larger ala nasi cartilage. Internally, by the nasal cavity, cartilages of the nasal septum lie adjacently with the inner surface of nasal bridge. Nasal septum cartilage is unpaired, has 4-angled polygon shape and forms a large frontal part of the nasal septum. In the rear and above the cartilage of the nasal septum connects with the perpendicular plate of the ethmoid bone, and in the rear and below it does so with the vomer and the frontal nasal spine. Between the lower edge of the cartilage of the nasal septum and the front edge of the vomer there is a narrow strip of the vomeronasal cartilage situated on each side. Apertura piriformis nasi comes in in its front, and paired holes, choanae, connect it to the nasopharynx from behind. Nasal cavity is divided into two not quite symmetrical halves with the bone of the nasal septum, septum nasi osseum. Each half of the nasal cavity has five walls: top wall, bottom wall, rear wall, medial wall and lateral wall. Figure 22 The nasal cavity 1 - paries superior; 2 - ostium pharyngeum tubae auditivae; 3 - palatum durum; 4 - palatum molle The upper wall of the nasal cavity is formed by a small part of the frontal bone, lamina cribrosa of the ethmoid bone and part of sphenoid bone. The bottom wall of the nasal cavity, or bottom, includes palatine process of the maxilla and the horizontal plate of the palatine bone that together form up the hard palate, palatum osseum. The rear wall of the nasal cavity goes only to a small extent and is present only in the upper section since otherwise it would block hoanas lying below. It is formed by the nasal surface of the body of the sphenoid bone with the twin foramens present on it – apertura sinus sphenoidalis. Lateral wall of the nasal cavity is formed by the lacrimal bone, os lacrimale, and lamina orbitalis of the ethmoid bone which together separate the nasal cavity from the eye socket. Nasal surface of the frontal process of the upper jaw and the thin bony plate separating the nasal cavity from the maxillary sinus, sinus maxillaris, also take part in the formation. There are three conches hanging down on the lateral wall of nasal cavity, They separate three nasal passages from each other: the upper passage, the middle passage and the lower passage. The upper nasal passage, meatus nasi superior, is located between the upper and middle conches of the ethmoid bone; the is half as long as the average passage and is located only in the posterior part of the nasal cavity; it communicates with sinus sphenoidalis, foramen sphenopalatinum. Middle nasal passage, meatus nasi medius, goes between the middle and lower conches. Cellulae ethmoidales anteriores et mediae and sinus maxillaris are also opened inside. The lower nasal passage, meatus nasi inferior, passes between the lower conch and the bottom of the nasal cavity. The space between the conches and nasal septum is marked as a common nasal passage. On the side wall of the nasopharynx there is a pharyngeal opening of the auditory tube that connects the pharyngeal cavity with the middle ear (tympanic cavity). The vessels of the nasal cavity form the anastomotic nets which are created by multiple systems. Really dense venous plexus (which look like cavernous formations) are swarmed under the mucosal tissue of the lower and middle conches. Veins of nasal cavity make anastomoses with the veins of the nasopharynx, orbits and the brain tunicas. Sensory innervation of the nasal mucosa is being done through the 1st and the 2nd branches of the trigeminal nerve, that is, optical and maxillary nerve. There are maxillary and frontal sinus, ethmoid labyrinth and partly sphenoid sinus present on each side of the nasal cavity. Its is the largest sinus among all the paranasal sinuses; its capacity in adults varies from 10 to 12 cm3 (Fig. The shape of the maxillary sinus resembles the tetrahedral pyramid whose base lies on the lateral wall of the nasal cavity, and the tip points at the zygomatic process of the maxilla. Figure 23 Variants of pneumatization of maxillar sinuses depending of maxilla structure: 1 - maxilla; 2 - sinus frontales; 3 - cellulae labyrinthus ethmoidalis; 4 - sinus maxillaris The anterior wall faces forward, top, or orbital, sinus wall separates the sinus from the eye sockets, and the posterior wall faces the infratemporal and pterygopalatine-palatal fossae. The bottom wall of the maxillary sinus is formed by the alveolar bone of the upper jaw, which separates sinus from the oral cavity. The inner, or nasal, sinus wall corresponds to the biggest part of the lower and middle nasal passages. The foramen, through which the maxillary sinus communicates with the nasal cavity, hiatus maxillaris, is located right beneath the bottom of the orbit. Such location contributes to the stagnation of the liquids excreted during sinus inflammations. The nasolacrimal duct goes across the anterior part of the inner wall of the sinus maxillaris, while celluli ethmoidali attach to the upper posterior part. The upper or orbital wall of the maxillary sinus is the thinnest one, especially in the posterior part. The frontal or the facial wall of the maxillary sinus of the upper jaw is formed by the part located between the infraorbital margin and alveolar process. It is the thickest wall of the maxillary sinus; it is covered with soft cheeck tissue and it can be easily palpated. The flat imprint in the center of the front surface of the anterior wall, which is called “fossa canina”, is the thinnest part of this wall. At the upper edge of the “fossa canina” threre is a foramen of the infraorbital nerve, foramen infraorbitale. The bottom wall, or bottom of the maxillary sinus, is located near the posterior part of the alveolar bone of the upper jaw and usually corresponds to the fossae of four upper posterior teeth. Frontal sinus, sinus frontalis, is located between the plates of orbital part and the squama of the frontal bone. It is divided into lower or orbital, anterior or front, back or brain, and the median walls. Frontal sinus communicates with the nasal cavity through the apertura sinus frontalis, which opens in front part of the middle nasal meatus. Sphenoid sinus, or sinus sphenoidalis, is located within the body of the sphenoid bone directly behind the ethmoid labyrinth above choanas and fornix pharyngis. The sinus with the sagital septum is divided into two unequal (in most cases) parts.