document_title: Wound healing

question_text: which phase of healing begins about 3 weeks after injury

question_tokens: which phase of healing begins about 3 weeks after injury

root

text: Wound healing

text: Timing and reepithelialization[edit]

text: Timing is important to wound healing. Critically, the timing of wound reepithelialization can decide the outcome of the healing.[11] If the epithelization of tissue over a denuded area is slow, a scar will form over many weeks, or months;[12][13] If the epithelization of a wounded area is fast, the healing will result in regeneration.[13]

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text: Early vs cellular phase[edit]

text: Wound healing is classically divided into hemostasis, inflammation, proliferation, and remodeling. Although a useful construct, this model employs considerable overlapping among individual phases. A complementary model has recently been described[1] where the many elements of wound healing are more clearly delineated. The importance of this new model becomes more apparent through its utility in the fields of regenerative medicine and tissue engineering (see Research and development section below). In this construct, the process of wound healing is divided into two major phases: the early phase and the cellular phase:[1]

text: The early phase, which begins immediately following skin injury, involves cascading molecular and cellular events leading to hemostasis and formation of an early, makeshift extracellular matrix that provides structural staging for cellular attachment and subsequent cellular proliferation.

text: The cellular phase involves several types of cells working together to mount an inflammatory response, synthesize granulation tissue, and restore the epithelial layer.[1] Subdivisions of the cellular phase are: [1] Macrophages and inflammatory components (within 1–2 days), [2] Epithelial-mesenchymal interaction: re-epithelialization (phenotype change within hours, migration begins on day 1 or 2), [3] Fibroblasts and myofibroblasts: progressive alignment, collagen production, and matrix contraction (between day 4 and day 14), [4] Endothelial cells and angiogenesis (begins on day 4), [5] Dermal matrix: elements of fabrication (begins on day 4, lasting 2 weeks) and alteration/remodeling (begins after week 2, lasting weeks to months—depending on wound size).[1]

text: Inflammatory phase[edit]

text: Just before the inflammatory phase is initiated, the clotting cascade occurs in order to achieve hemostasis, or stop blood loss by way of a fibrin clot. Thereafter, various soluble factors (including chemokines and cytokines) are released to attract cells that phagocytise debris, bacteria, and damaged tissue, in addition to releasing signaling molecules that initiate the proliferative phase of wound healing.

text: Clotting cascade[edit]

text: When tissue is first wounded, blood comes in contact with collagen, triggering blood platelets to begin secreting inflammatory factors.[15] Platelets also express sticky glycoproteins on their cell membranes that allow them to aggregate, forming a mass.[6]

text: Fibrin and fibronectin cross-link together and form a plug that traps proteins and particles and prevents further blood loss.[16] This fibrin-fibronectin plug is also the main structural support for the wound until collagen is deposited.[6] Migratory cells use this plug as a matrix to crawl across, and platelets adhere to it and secrete factors.[6] The clot is eventually lysed and replaced with granulation tissue and then later with collagen.

text: Platelets, the cells present in the highest numbers shortly after a wound occurs, release mediators into the blood, including cytokines and growth factors.[15] Growth factors stimulate cells to speed their rate of division. Platelets release other proinflammatory factors like serotonin, bradykinin, prostaglandins, prostacyclins, thromboxane, and histamine,[3] which serve several purposes, including increasing cell proliferation and migration to the area and causing blood vessels to become dilated and porous. In many ways, extravasated platelets in trauma perform a similar function to tissue macrophages and mast cells exposed to microbial molecular signatures in infection: they become activated, and secrete molecular mediators – vasoactive amines, eicosanoids, and cytokines – that initiate the inflammatory process.

text: Vasoconstriction and vasodilation[edit]

text: Immediately after a blood vessel is breached, ruptured cell membranes release inflammatory factors like thromboxanes and prostaglandins that cause the vessel to spasm to prevent blood loss and to collect inflammatory cells and factors in the area.[3] This vasoconstriction lasts five to ten minutes and is followed by vasodilation, a widening of blood vessels, which peaks at about 20 minutes post-wounding.[3] Vasodilation is the end result of factors released by platelets and other cells. The main factor involved in causing vasodilation is histamine.[3][15] Histamine also causes blood vessels to become porous, allowing the tissue to become edematous because proteins from the bloodstream leak into the extravascular space, which increases its osmolar load and draws water into the area.[3] Increased porosity of blood vessels also facilitates the entry of inflammatory cells like leukocytes into the wound site from the bloodstream.[17][18]

text: Polymorphonuclear neutrophils[edit]

text: Within an hour of wounding, polymorphonuclear neutrophils (PMNs) arrive at the wound site and become the predominant cells in the wound for the first two days after the injury occurs, with especially high numbers on the second day.[19] They are attracted to the site by fibronectin, growth factors, and substances such as kinins. Neutrophils phagocytise debris and kill bacteria by releasing free radicals in what is called a 'respiratory burst.[20][21] They also cleanse the wound by secreting proteases that break down damaged tissue. Functional neutrophils at the wound site only have life-spans of around 2 days, so they usually undergo apoptosis once they have completed their tasks and are engulfed and degraded by macrophages.[22]

text: Other leukocytes to enter the area include helper T cells, which secrete cytokines to cause more T cells to divide and to increase inflammation and enhance vasodilation and vessel permeability.[17][23] T cells also increase the activity of macrophages.[17]

text: Macrophages[edit]

text: One of the macrophage's roles is to phagocytize other expended phagocytes,[24] bacteria and damaged tissue,[19] and they also debride damaged tissue by releasing proteases.[25]

text: Macrophages function in regeneration[26][27] and are essential for wound healing.[19] They are stimulated by the low oxygen content of their surroundings to produce factors that induce and speed angiogenesis[20] and they also stimulate cells that reepithelialize the wound, create granulation tissue, and lay down a new extracellular matrix.[28][29] By secreting these factors, macrophages contribute to pushing the wound healing process into the next phase. They replace PMNs as the predominant cells in the wound by two days after injury.[24]

text: The spleen contains half the body's monocytes in reserve ready to be deployed to injured tissue.[30][31] Attracted to the wound site by growth factors released by platelets and other cells, monocytes from the bloodstream enter the area through blood vessel walls.[32] Numbers of monocytes in the wound peak one to one and a half days after the injury occurs.[23] Once they are in the wound site, monocytes mature into macrophages. Macrophages also secrete a number of factors such as growth factors and other cytokines, especially during the third and fourth post-wounding days. These factors attract cells involved in the proliferation stage of healing to the area.[15]

text: In wound healing that result in incomplete repair, scar contraction occurs, bringing varying gradations of structural imperfections, deformities and problems with flexibility.[33] Macrophages may restrain the contraction phase.[27] Scientists have reported that removing the macrophages from a salamander resulted in failure of a typical regeneration response (limb regeneration), instead bringing on a repair (scarring) response.[34][35]

text: Decline of inflammatory phase[edit]

text: As inflammation dies down, fewer inflammatory factors are secreted, existing ones are broken down, and numbers of neutrophils and macrophages are reduced at the wound site.[19] These changes indicate that the inflammatory phase is ending and the proliferative phase is underway.[19] In vitro evidence, obtained using the dermal equivalent model, suggests that the presence of macrophages actually delays wound contraction and thus the disappearance of macrophages from the wound may be essential for subsequent phases to occur.[27]

text: Because inflammation plays roles in fighting infection, clearing debris and inducing the proliferation phase, it is a necessary part of healing. However, inflammation can lead to tissue damage if it lasts too long.[6] Thus the reduction of inflammation is frequently a goal in therapeutic settings. Inflammation lasts as long as there is debris in the wound. Thus, if the individual's immune system is compromised and is unable to clear the debris from the wound and/or if excessive detritus, devitalized tissue, or microbial biofilm is present in the wound, these factors may cause a prolonged inflammatory phase and prevent the wound from properly commencing the proliferation phase of healing. This can lead to a chronic wound.

text: Proliferative phase[edit]

text: About two or three days after the wound occurs, fibroblasts begin to enter the wound site, marking the onset of the proliferative phase even before the inflammatory phase has ended.[36] As in the other phases of wound healing, steps in the proliferative phase do not occur in a series but rather partially overlap in time.

text: Angiogenesis[edit]

text: Also called neovascularization, the process of angiogenesis occurs concurrently with fibroblast proliferation when endothelial cells migrate to the area of the wound.[37] Because the activity of fibroblasts and epithelial cells requires oxygen and nutrients, angiogenesis is imperative for other stages in wound healing, like epidermal and fibroblast migration. The tissue in which angiogenesis has occurred typically looks red (is erythematous) due to the presence of capillaries.[37]

text: Angiogenesis occurs in overlapping phases in response to inflammation:

text:
Latent period: During the haemostatic and inflammatory phase of the wound healing process, vasodilation and permeabilisation allow leukocyte extravasation and phagocytic debridement and decontamination of the wound area. Tissue swelling aids later angiogenesis by expanding and loosening the existing collagenous extracellular matrix.
Endothelial activation: As the wound macrophages switches from inflammatory to healing mode, it begins to secrete endothelial chemotactic and growth factors to attract adjacent endothelial cells. Activated endothelial cells respond by retracting and reducing cell junctions, loosening themselves from their embedded endothelium. Characteristically the activated endothelial cells show enlarged nucleoli.
Degradation of endothelial basement membrane: The wound macrophages, mast cells and the endothelial cells themselves secrete proteases to break down existing vascular basal lamina.
Vascular sprouting: With the breakdown of endothelial basement membrane, detached endothelial cells from pre-existing capillaries and post-capillary venues can divide and migrate chemotactically towards the wound, laying down new vessels in the process. Vascular sprouting can be aided by ambient hypoxia and acidosis in the wound environment, as hypoxia stimulates the endothelial transcription factor, hypoxia inducible factor (HIF) to transactivate angiogenic genes such as VEGF and GLUT1. Sprouted vessels can self-organise into luminal morphologies, and fusion of blind channels give rise to new capillary networks.
Vascular maturation: the endothelium of vessels mature by laying down new endothelial extracellular matrix, followed by basal lamina formation. Lastly the vessel establishes a pericyte layer.

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text: Stem cells of endothelial cells, originating from parts of uninjured blood vessels, develop pseudopodia and push through the ECM into the wound site to establish new blood vessels.[20]

text: Endothelial cells are attracted to the wound area by fibronectin found on the fibrin scab and chemotactically by angiogenic factors released by other cells,[38] e.g. from macrophages and platelets when in a low-oxygen environment. Endothelial growth and proliferation is also directly stimulated by hypoxia, and presence of lactic acid in the wound.[36] For example, hypoxia stimulates the endothelial transcription factor, hypoxia-inducible factor (HIF) to transactivate a set of proliferative genes including vascular endothelial growth factor (VEGF) and glucose transporter 1 (GLUT1).

text: To migrate, endothelial cells need collagenases and plasminogen activator to degrade the clot and part of the ECM.[3][19] Zinc-dependent metalloproteinases digest basement membrane and ECM to allow cell migration, proliferation and angiogenesis.[39]

text: When macrophages and other growth factor-producing cells are no longer in a hypoxic, lactic acid-filled environment, they stop producing angiogenic factors.[20] Thus, when tissue is adequately perfused, migration and proliferation of endothelial cells is reduced. Eventually blood vessels that are no longer needed die by apoptosis.[38]

text: Fibroplasia and granulation tissue formation[edit]

text: Simultaneously with angiogenesis, fibroblasts begin accumulating in the wound site. Fibroblasts begin entering the wound site two to five days after wounding as the inflammatory phase is ending, and their numbers peak at one to two weeks post-wounding.[19] By the end of the first week, fibroblasts are the main cells in the wound.[3] Fibroplasia ends two to four weeks after wounding.

text: As a model the mechanism of fibroplasia may be conceptualised as an analogous process to angiogenesis (see above) - only the cell type involved is fibroblasts rather than endothelial cells. Initially there is a latent phase where the wound undergoes plasma exudation, inflammatory decontamination and debridement. Oedema increases the wound histologic accessibility for later fibroplastic migration. Second, as inflammation nears completion, macrophage and mast cells release fibroblast growth and chemotactic factors to activate fibroblasts from adjacent tissue. Fibroblasts at this stage loosen themselves from surrounding cells and ECM. Phagocytes further release proteases that break down the ECM of neighbouring tissue, freeing the activated fibroblasts to proliferate and migrate towards the wound. The difference between vascular sprouting and fibroblast proliferation is that the former is enhanced by hypoxia, whilst the latter is inhibited by hypoxia. The deposited fibroblastic connective tissue matures by secreting ECM into the extracellular space, forming granulation tissue (see below). Lastly collagen is deposited into the ECM.

text: In the first two or three days after injury, fibroblasts mainly migrate and proliferate, while later, they are the main cells that lay down the collagen matrix in the wound site.[3] Origins of these fibroblasts are thought to be from the adjacent uninjured cutaneous tissue (although new evidence suggests that some are derived from blood-borne, circulating adult stem cells/precursors).[40] Initially fibroblasts utilize the fibrin cross-linking fibers (well-formed by the end of the inflammatory phase) to migrate across the wound, subsequently adhering to fibronectin.[38] Fibroblasts then deposit ground substance into the wound bed, and later collagen, which they can adhere to for migration.[15]

text: Granulation tissue functions as rudimentary tissue, and begins to appear in the wound already during the inflammatory phase, two to five days post wounding, and continues growing until the wound bed is covered. Granulation tissue consists of new blood vessels, fibroblasts, inflammatory cells, endothelial cells, myofibroblasts, and the components of a new, provisional extracellular matrix (ECM). The provisional ECM is different in composition from the ECM in normal tissue and its components originate from fibroblasts.[28] Such components include fibronectin, collagen, glycosaminoglycans, elastin, glycoproteins and proteoglycans.[38] Its main components are fibronectin and hyaluronan, which create a very hydrated matrix and facilitate cell migration.[32] Later this provisional matrix is replaced with an ECM that more closely resembles that found in non-injured tissue.

text: Growth factors (PDGF, TGF-β) and fibronectin encourage proliferation, migration to the wound bed, and production of ECM molecules by fibroblasts. Fibroblasts also secrete growth factors that attract epithelial cells to the wound site. Hypoxia also contributes to fibroblast proliferation and excretion of growth factors, though too little oxygen will inhibit their growth and deposition of ECM components, and can lead to excessive, fibrotic scarring.

text: Collagen deposition[edit]

text: One of fibroblasts' most important duties is the production of collagen.[37]

text: Collagen deposition is important because it increases the strength of the wound; before it is laid down, the only thing holding the wound closed is the fibrin-fibronectin clot, which does not provide much resistance to traumatic injury.[20] Also, cells involved in inflammation, angiogenesis, and connective tissue construction attach to, grow and differentiate on the collagen matrix laid down by fibroblasts.[41]

text: Type III collagen and fibronectin generally begin to be produced in appreciable amounts at somewhere between approximately 10 hours[42] and 3 days,[38] depending mainly on wound size. Their deposition peaks at one to three weeks.[28] They are the predominating tensile substances until the later phase of maturation, in which they are replaced by the stronger type I collagen.

text: Even as fibroblasts are producing new collagen, collagenases and other factors degrade it. Shortly after wounding, synthesis exceeds degradation so collagen levels in the wound rise, but later production and degradation become equal so there is no net collagen gain.[20] This homeostasis signals the onset of the later maturation phase. Granulation gradually ceases and fibroblasts decrease in number in the wound once their work is done.[43] At the end of the granulation phase, fibroblasts begin to commit apoptosis, converting granulation tissue from an environment rich in cells to one that consists mainly of collagen.[3]

text: Epithelialization[edit]

text: The formation of granulation tissue into an open wound allows the reepithelialization phase to take place, as epithelial cells migrate across the new tissue to form a barrier between the wound and the environment.[38] Basal keratinocytes from the wound edges and dermal appendages such as hair follicles, sweat glands and sebacious (oil) glands are the main cells responsible for the epithelialization phase of wound healing.[43] They advance in a sheet across the wound site and proliferate at its edges, ceasing movement when they meet in the middle. In healing that results in a scar, sweat glands, hair follicles[44][45] and nerves do not form. With the lack of hair follicles, nerves and sweat glands, the wound, and the resulting healing scar, provide a challenge to the body with regards to temperature control.[45]

text: Keratinocytes migrate without first proliferating.[46] Migration can begin as early as a few hours after wounding. However, epithelial cells require viable tissue to migrate across, so if the wound is deep it must first be filled with granulation tissue.[47] Thus the time of onset of migration is variable and may occur about one day after wounding.[48] Cells on the wound margins proliferate on the second and third day post-wounding in order to provide more cells for migration.[28]

text: If the basement membrane is not breached, epithelial cells are replaced within three days by division and upward migration of cells in the stratum basale in the same fashion that occurs in uninjured skin.[38] However, if the basement membrane is ruined at the wound site, reepithelization must occur from the wound margins and from skin appendages such as hair follicles and sweat and oil glands that enter the dermis that are lined with viable keratinocytes.[28] If the wound is very deep, skin appendages may also be ruined and migration can only occur from wound edges.[47]

text: Migration of keratinocytes over the wound site is stimulated by lack of contact inhibition and by chemicals such as nitric oxide.[49] Before they begin to migrate, cells must dissolve their desmosomes and hemidesmosomes, which normally anchor the cells by intermediate filaments in their cytoskeleton to other cells and to the ECM.[23] Transmembrane receptor proteins called integrins, which are made of glycoproteins and normally anchor the cell to the basement membrane by its cytoskeleton, are released from the cell's intermediate filaments and relocate to actin filaments to serve as attachments to the ECM for pseudopodia during migration.[23] Thus keratinocytes detach from the basement membrane and are able to enter the wound bed.[36]

text: Before they begin migrating, keratinocytes change shape, becoming longer and flatter and extending cellular processes like lamellipodia and wide processes that look like ruffles.[32] Actin filaments and pseudopodia form.[36] During migration, integrins on the pseudopod attach to the ECM, and the actin filaments in the projection pull the cell along.[23] The interaction with molecules in the ECM through integrins further promotes the formation of actin filaments, lamellipodia, and filopodia.[23]

text: Epithelial cells climb over one another in order to migrate.[43] This growing sheet of epithelial cells is often called the epithelial tongue.[46] The first cells to attach to the basement membrane form the stratum basale. These basal cells continue to migrate across the wound bed, and epithelial cells above them slide along as well.[46] The more quickly this migration occurs, the less of a scar there will be.[50]

text: Fibrin, collagen, and fibronectin in the ECM may further signal cells to divide and migrate. Like fibroblasts, migrating keratinocytes use the fibronectin cross-linked with fibrin that was deposited in inflammation as an attachment site to crawl across.[25][32][43]

text: As keratinocytes migrate, they move over granulation tissue but stay underneath the scab, thereby separating the scab from the underlying tissue.[43][48] Scabs are formed on locations that are exposed to harmful UVR and the main biological function of human wound scabs is to inhibit the exposure to UVR, thus protecting otherwise exposed cells in a wound from UVR-induced DNA damage.[51] Epithelial cells have the ability to phagocytize debris such as dead tissue and bacterial matter that would otherwise obstruct their path. Because they must dissolve any scab that forms, keratinocyte migration is best enhanced by a moist environment, since a dry one leads to formation of a bigger, tougher scab.[25][38][43][52] To make their way along the tissue, keratinocytes must dissolve the clot, debris, and parts of the ECM in order to get through.[48][53] They secrete plasminogen activator, which activates plasminogen, turning it into plasmin to dissolve the scab. Cells can only migrate over living tissue,[43] so they must excrete collagenases and proteases like matrix metalloproteinases (MMPs) to dissolve damaged parts of the ECM in their way, particularly at the front of the migrating sheet.[48] Keratinocytes also dissolve the basement membrane, using instead the new ECM laid down by fibroblasts to crawl across.[23]

text: As keratinocytes continue migrating, new epithelial cells must be formed at the wound edges to replace them and to provide more cells for the advancing sheet.[25] Proliferation behind migrating keratinocytes normally begins a few days after wounding[47] and occurs at a rate that is 17 times higher in this stage of epithelialization than in normal tissues.[25] Until the entire wound area is resurfaced, the only epithelial cells to proliferate are at the wound edges.[46]

text: Growth factors, stimulated by integrins and MMPs, cause cells to proliferate at the wound edges. Keratinocytes themselves also produce and secrete factors, including growth factors and basement membrane proteins, which aid both in epithelialization and in other phases of healing.[54] Growth factors are also important for the innate immune defense of skin wounds by stimulation of the production of antimicrobial peptides and neutrophil chemotactic cytokines in keratinocytes.

text: Keratinocytes continue migrating across the wound bed until cells from either side meet in the middle, at which point contact inhibition causes them to stop migrating.[32] When they have finished migrating, the keratinocytes secrete the proteins that form the new basement membrane.[32] Cells reverse the morphological changes they underwent in order to begin migrating; they reestablish desmosomes and hemidesmosomes and become anchored once again to the basement membrane.[23] Basal cells begin to divide and differentiate in the same manner as they do in normal skin to reestablish the strata found in reepithelialized skin.[32]

text: Contraction[edit]

text: Contraction is a key phase of wound healing with repair. If contraction continues for too long, it can lead to disfigurement and loss of function.[33] Thus there is a great interest in understanding the biology of wound contraction, which can be modelled in vitro using the collagen gel contraction assay or the dermal equivalent model.[27][55]

text: Contraction commences approximately a week after wounding, when fibroblasts have differentiated into myofibroblasts.[56] In full thickness wounds, contraction peaks at 5 to 15 days post wounding.[38] Contraction can last for several weeks[47] and continues even after the wound is completely reepithelialized.[3] A large wound can become 40 to 80% smaller after contraction.[32][43] Wounds can contract at a speed of up to 0.75 mm per day, depending on how loose the tissue in the wounded area is.[38] Contraction usually does not occur symmetrically; rather most wounds have an 'axis of contraction' which allows for greater organization and alignment of cells with collagen.[56]

text: At first, contraction occurs without myofibroblast involvement.[57] Later, fibroblasts, stimulated by growth factors, differentiate into myofibroblasts. Myofibroblasts, which are similar to smooth muscle cells, are responsible for contraction.[57] Myofibroblasts contain the same kind of actin as that found in smooth muscle cells.[33]

text: Myofibroblasts are attracted by fibronectin and growth factors and they move along fibronectin linked to fibrin in the provisional ECM in order to reach the wound edges.[25] They form connections to the ECM at the wound edges, and they attach to each other and to the wound edges by desmosomes. Also, at an adhesion called the fibronexus, actin in the myofibroblast is linked across the cell membrane to molecules in the extracellular matrix like fibronectin and collagen.[57] Myofibroblasts have many such adhesions, which allow them to pull the ECM when they contract, reducing the wound size.[33] In this part of contraction, closure occurs more quickly than in the first, myofibroblast-independent part.[57]

text: As the actin in myofibroblasts contracts, the wound edges are pulled together. Fibroblasts lay down collagen to reinforce the wound as myofibroblasts contract.[3] The contraction stage in proliferation ends as myofibroblasts stop contracting and commit apoptosis.[33] The breakdown of the provisional matrix leads to a decrease in hyaluronic acid and an increase in chondroitin sulfate, which gradually triggers fibroblasts to stop migrating and proliferating.[19] These events signal the onset of the maturation stage of wound healing.

text: Maturation and remodeling[edit]

text: When the levels of collagen production and degradation equalize, the maturation phase of tissue repair is said to have begun.[20] During maturation, type III collagen, which is prevalent during proliferation, is replaced by type I collagen.[17] Originally disorganized collagen fibers are rearranged, cross-linked, and aligned along tension lines.[32] The onset of the maturation phase may vary extensively, depending on the size of the wound and whether it was initially closed or left open,[28] ranging from approximately 3 days[42] to 3 weeks.[58] The maturation phase can last for a year or longer, similarly depending on wound type.[28]

text: As the phase progresses, the tensile strength of the wound increases.[28] Collagen will reach approximately 20% of its tensile strength after 3 weeks, increasing to 80% by 12th week. The maximum scar strength is 80% of that of unwounded skin.[59] Since activity at the wound site is reduced, the scar loses its red appearance as blood vessels that are no longer needed are removed by apoptosis.[20]

text: The phases of wound healing normally progress in a predictable, timely manner; if they do not, healing may progress inappropriately to either a chronic wound [6] such as a venous ulcer or pathological scarring such as a keloid scar.[60][61]

text: Factors affecting wound healing[edit]

text: Many factors controlling the efficacy, speed, and manner of wound healing fall under two types: local and systemic factors.[2]

text: Local factors[edit]

text:
Moisture; keeping a wound moist rather than dry makes wound healing more rapid and with less pain and less scarring[62]
Mechanical factors
Edema
Ionizing radiation
Faculty technique of wound closure
Ischemia and necrosis
Foreign bodies. Sharp, small foreign bodies can penetrate the skin leaving little surface wound but causing internal injury and internal bleeding. For a glass foreign body, "frequently, an innocent skin wound disguises the extensive nature of the injuries beneath".[63] First-degree nerve injury requires a few hours to a few weeks to recover.[64] If a foreign body passes by a nerve and causes first-degree nerve injury during entry, then the sensation of the foreign body or pain due to internal wounding may be delayed by a few hours to a few weeks after entry. A sudden increase in pain during the first few weeks of wound healing could be a sign of a recovered nerve reporting internal injuries rather than a newly developed infection.
Low oxygen tension
Perfusion

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text: Systemic factors[edit]

text:
Inflammation
Diabetes – Individuals with diabetes demonstrate reduced capability in the healing of acute wounds. Additionally, diabetic individuals are susceptible to developing chronic diabetic foot ulcers, a serious complication of diabetes which affects 15% of people with diabetes and accounts for 84% of all diabetes-related lower leg amputations.[65] The impaired healing abilities of diabetics with diabetic foot ulcers and/or acute wounds involves multiple pathophysiological mechanisms.[66] This impaired healing involves hypoxia, fibroblast and epidermal cell dysfunction, impaired angiogenesis and neovascularization, high levels of metalloproteases, damage from reactive oxygen species and AGEs (advanced glycation end-products), decreased host immune resistance, and neuropathy.[66]
Nutrients – Malnutrition or nutritional deficiencies have a recognizable impact on wound healing post trauma or surgical intervention.[67] Nutrients including proteins, carbohydrates, arginine, glutamine, polyunsaturated fatty acids, vitamin A, vitamin C, vitamin E, magnesium, copper, zinc and iron all play significant roles in wound healing.[66] Fats and carbohydrates provide the majority of energy required for wound healing. Glucose is the most prominent source of fuel and it is used to create cellular ATP, providing energy for angiogenesis and the deposition of new tissues.[68] As the nutritional needs of each patient and their associated wound are complex, it is suggested that tailored nutritional support would benefit both acute and chronic wound healing.[66]
Metabolic diseases
Immunosuppression
Connective tissue disorders
Smoking Smoking causes a delay in the speed of wound repair notably in the proliferative and inflammatory phases. It also increases the likelihood of certain complications such as wound rupture, wound and flap necrosis, decrease in wound tensile strength and infection.[68]
Age – Increased age (over 60 years) is a risk factor for impaired wound healing.[66] It is recognized that, in older adults of otherwise overall good health, the effects of aging causes a temporal delay in healing, but no major impairment with regard to the quality of healing.[69] Delayed wound healing in patients of increasing age is associated with altered inflammatory response; for example delayed T-cell infiltration of the wound with alterations in the production of chemokines, and reduced macrophage phagocytic capacity.[70]
Alcohol – Alcohol consumption impairs wound healing and also increases the chances of infection. Alcohol affects the proliferative phase of healing. A single unit of alcohol causes a negative effect on re-epithelialization, wound closure, collagen production and angiogenesis.[68]

text: Research and development[edit]

text: Up until a decade ago,[when?] the classic paradigm of wound healing, involving stem cells restricted to organ-specific lineages, had never been seriously challenged. Since then,[when?] the notion of adult stem cells having cellular plasticity or the ability to differentiate into non-lineage cells has emerged as an alternative explanation.[1] To be more specific, hematopoietic progenitor cells (that give rise to mature cells in the blood) may have the ability de-differentiate back into hematopoietic stem cells and/or transdifferentiate into non-lineage cells, such as fibroblasts.[40]

text: Stem cells and cellular plasticity[edit]

text: Multipotent adult stem cells have the capacity to be self-renewing and give rise to different cell types. Stem cells give rise to progenitor cells, which are cells that are not self-renewing, but can generate several types of cells. The extent of stem cell involvement in cutaneous (skin) wound healing is complex and not fully understood.

text: It is thought that the epidermis and dermis are reconstituted by mitotically active stem cells that reside at the apex of rete ridges (basal stem cells or BSC), the bulge of hair follicles (hair follicular stem cell or HFSC), and the papillary dermis (dermal stem cells).[1] Moreover, bone marrow may also contain stem cells that play a major role in cutaneous wound healing.[40]

text: In rare circumstances, such as extensive cutaneous injury, self-renewal subpopulations in the bone marrow are induced to participate in the healing process, whereby they give rise to collagen-secreting cells that seem to play a role during wound repair.[1] These two self-renewal subpopulations are (1) bone marrow-derived mesenchymal stem cells (MSC) and (2) hematopoietic stem cells (HSC). Bone marrow also harbors a progenitor subpopulation (endothelial progenitor cells or EPC) that, in the same type of setting, are mobilized to aid in the reconstruction of blood vessels.[40] Moreover, it thought that, extensive injury to skin also promotes the early trafficking of a unique subclass of leukocytes (circulating fibrocytes) to the injured region, where they perform various functions related to wound healing.[1]

text: Wound repair versus regeneration[edit]

text: An injury is an interruption of morphology and/or functionality of a given tissue. After injury, structural tissue heals with incomplete or complete regeneration.[71][72] Whereas, tissue without an interruption to the morphology almost always completely regenerates. An example of complete regeneration without an interruption of the morphology is non-injured tissue, such as skin.[73] Non-injured skin has a continued replacement and regeneration of cells which always results in complete regeneration.[73]

text: There is a subtle distinction between 'repair' and 'regeneration'.[1][71][72] Repair means incomplete regeneration.[71] Repair or incomplete regeneration, refers to the physiologic adaptation of an organ after injury in an effort to re-establish continuity without regards to exact replacement of lost/damaged tissue.[71] True tissue regeneration or complete regeneration,[72] refers to the replacement of lost/damaged tissue with an ‘exact’ copy, such that both morphology and functionality are completely restored.[72] Though after injury mammals can completely regenerate spontaneously, they usually do not completely regenerate. An example of a tissue regenerating completely after an interruption of morphology is the endometrium; the endometrium after the process of breakdown via the menstruation cycle heals with complete regeneration.[73]

text: In some instances, after a tissue breakdown, such as in skin, a regeneration closer to complete regeneration may be induced by the use of biodegradable (collagen-glycoaminoglycan) scaffolds. These scaffolds are structurally analogous to extracellular matrix (ECM) found in normal/un-injured dermis.[74] Interestingly, fundamental conditions required for tissue regeneration often oppose conditions that favor efficient wound repair, including inhibition of (1) platelet activation, (2) inflammatory response, and (3) wound contraction.[1] In addition to providing support for fibroblast and endothelial cell attachment, biodegradable scaffolds inhibit wound contraction, thereby allowing the healing process to proceed towards a more-regenerative/less-scarring pathway. Pharmaceutical agents have been investigated which may be able to turn off myofibroblast differentiation.[75]

text: A new way of thinking derived from the notion that heparan sulfates are key player in tissue homeostasis: the process that makes the tissue replace dead cells by identical cells. In wound areas, tissue homeostasis is lost as the heparan sulfates are degraded preventing the replacement of dead cells by identical cells. Heparan sulfate analogues cannot be degraded by all know heparanases and glycanases and bind to the free heparin sulfate binding spots on the ECM, therefore preserving the normal tissue homeostasis and preventing scarring.[76][77][78]

text: Repair or regeneration with regards to hypoxia-inducible factor 1-alpha (HIF-1a). In normal circumstances after injury HIF-1a is degraded by prolyl hydroxylases (PHDs). Scientists found that the simple up-regulation of HIF-1a via PHD inhibitors regenerates lost or damaged tissue in mammals that have a repair response; and the continued down-regulation of Hif-1a results in healing with a scarring response in mammals with a previous regenerative response to the loss of tissue. The act of regulating HIF-1a can either turn off, or turn on the key process of mammalian regeneration.[79][80]

text: Scarless wound healing[edit]

text: Scarless wound healing is a concept based on the healing or repair of the skin (or other tissue/organs) after injury with the aim of healing with subjectively and relatively less scar tissue than normally expected. Scarless healing is sometimes mixed up with the concept of scar free healing, which is wound healing which results in absolutely no scar (free of scarring). However they are different concepts.

text: A reverse to scarless wound healing is scarification (wound healing to scar more). Historically, certain cultures consider scarification attractive;[81] however, this is generally not the case in the modern western society, in which many patients are turning to plastic surgery clinics with unrealistic expectations. Depending on scar type, treatment may be invasive (intralesional steroid injections, surgery) and/or conservative (compression therapy, topical silicone gel, brachytherapy, photodynamic therapy).[82] Clinical judgment is necessary to successfully balance the potential benefits of the various treatments available against the likelihood of a poor response and possible complications resulting from these treatments. Many of these treatments may only have a placebo effect, and the evidence base for the use of many current treatments is poor.[83]

text: Since the 1960s, comprehension of the basic biologic processes involved in wound repair and tissue regeneration have expanded due to advances in cellular and molecular biology.[84] Currently, the principal goals in wound management are to achieve rapid wound closure with a functional tissue that has minimal aesthetic scarring.[85] However, the ultimate goal of wound healing biology is to induce a more perfect reconstruction of the wound area. Scarless wound healing only occurs in mammalian foetal tissues [86] and complete regeneration is limited to lower vertebrates, such as salamanders, and invertebrates.[87] In adult humans, injured tissue are repaired by collagen deposition, collagen remodelling and eventual scar formation, where fetal wound healing is believed to be more of a regenerative process with minimal or no scar formation.[86] Therefore, foetal wound healing can be used to provide an accessible mammalian model of an optimal healing response in adult human tissues. Clues as to how this might be achieved come from studies of wound healing in embryos, where repair is fast and efficient and results in essentially perfect regeneration of any lost tissue.

text: The etymology of the term scarless wound healing has a long history.[88][89][90] In print the antiquated concept of scarless healing was brought up the early 20th century and appeared in a paper published in the London Lancet. This process involved cutting in a surgical slant, instead of a right angle…; it was described in various Newspapers.[88][89][90]

text: Simulating wound healing from a growth perspective[edit]

text: Considerable effort has been devoted to understanding the physical relationships governing wound healing and subsequent scarring, with mathematical models and simulations developed to elucidate these relationships.[91] The growth of tissue around the wound site is a result of the migration of cells and collagen deposition by these cells. The alignment of collagen describes the degree of scarring; basket-weave orientation of collagen is characteristic of normal skin, whereas aligned collagen fibers lead to significant scarring.[92] It has been shown that the growth of tissue and extent of scar formation can be controlled by modulating the stress at a wound site.[93]

text: The growth of tissue can be simulated using the aforementioned relationships from a biochemical and biomechanical point of view. The biologically active chemicals that play an important role in wound healing are modeled with Fickian diffusion to generate concentration profiles. The balance equation for open systems when modeling wound healing incorporates mass growth due to cell migration and proliferation. Here the following equation is used:

text: Dtρ0 = Div (R) + R0,

text: where ρ represents mass density, R represents a mass flux (from cell migration), and R0 represents a mass source (from cell proliferation, division, or enlargement).[94]

text: Wound closure intentions[edit]

text: Successful wound healing is dependent upon various cell types, molecular mediators and structural elements.[95]

text: Primary intention[edit]

text: Primary intention is the healing of a clean wound without tissue loss.[95] In this process, wound edges are brought together, so that they are adjacent to each other (re-approximated). Wound closure is performed with sutures (stitches), staples, or adhesive tape or glue.

text: Primary intention can only be implemented when the wound is precise and there is minimal disruption to the local tissue and the epithelial basement membrane e.g. surgical incisions.[96]

text: This process is faster than healing by secondary intention.[95] There is also less scarring associated with primary intention, as there are no large tissue losses to be filled with granulation tissue.[95] (primary intention do require some granulation tissue to form.)

text: Examples of primary intention include: well-repaired lacerations, well reduced bone fractures, healing after flap surgery.

text: Secondary intention[edit]

text:
Secondary intention is implemented when primary intention is not possible.
This is due to wounds being created by major trauma in which there has been a significant loss in tissue or tissue damage.[96]
The wound is allowed to granulate.
Surgeon may pack the wound with a gauze or use a drainage system.
Granulation results in a broader scar.
Healing process can be slow due to presence of drainage from infection.
Wound care must be performed daily to encourage wound debris removal to allow for granulation tissue formation.
Examples: gingivectomy, gingivoplasty, tooth extraction sockets, poorly reduced fractures, burns, severe lacerations, pressure ulcers.

text: Tertiary intention[edit]

text: (Delayed primary closure or secondary suture):

text:
The wound is initially cleaned, debrided and observed, typically 4 or 5 days before closure.
The wound is purposely left open
Examples: healing of wounds by use of tissue grafts.

text: If the wound edges are not reapproximated immediately, delayed primary wound healing transpires. This type of healing may be desired in the case of contaminated wounds. By the fourth day, phagocytosis of contaminated tissues is well underway, and the processes of epithelization, collagen deposition, and maturation are occurring. Foreign materials are walled off by macrophages that may metamorphose into epithelioid cells, which are encircled by mononuclear leukocytes, forming granulomas. Usually the wound is closed surgically at this juncture, and if the "cleansing" of the wound is incomplete, chronic inflammation can ensue, resulting in prominent scarring.

text: Overview of involved growth factors[edit]

text: Following are the main growth factors involved in wound healing:

text:
Growth factor
Abbreviation
Main origins
Effects

Epidermal growth factor
EGF

Activated macrophages
Salivary glands
Keratinocytes

Keratinocyte and fibroblast mitogen
Keratinocyte migration
Granulation tissue formation

Transforming growth factor-α
TGF-α

Activated macrophages
T-lymphocytes
Keratinocytes

Hepatocyte and epithelial cell proliferation
Expression of antimicrobial peptides
Expression of chemotactic cytokines

Hepatocyte growth factor
HGF

Mesenchymal cells

Epithelial and endothelial cell proliferation
Hepatocyte motility

Vascular endothelial growth factor
VEGF

Mesenchymal cells

Vascular permeability
Endothelial cell proliferation

Platelet derived growth factor
PDGF

Platelets
Macrophages
Endothelial cells
Smooth muscle cells
Keratinocytes

Granulocyte, macrophage, fibroblast and smooth muscle cell chemotaxis
Granulocyte, macrophage and fibroblast activation
Fibroblast, endothelial cell and smooth muscle cell proliferation
Matrix metalloproteinase, fibronectin and hyaluronan production
Angiogenesis
Wound remodeling
Integrin expression regulation

Fibroblast growth factor 1 and 2
FGF-1, −2

Macrophages
Mast cells
T-lymphocytes
Endothelial cells
Fibroblasts

Fibroblast chemotaxis
Fibroblast and keratinocyte proliferation
Keratinocyte migration
Angiogenesis
Wound contraction
Matrix (collagen fibers) deposition

Transforming growth factor-β
TGF-β

Platelets
T-lymphocytes
Macrophages
Endothelial cells
Keratinocytes
Smooth muscle cells
Fibroblasts

Granulocyte, macrophage, lymphocyte, fibroblast and smooth muscle cell chemotaxis
TIMP synthesis
Angiogenesis
Fibroplasia
Matrix metalloproteinase production inhibition
Keratinocyte proliferation

Keratinocyte growth factor
KGF

Keratinocytes

Keratinocyte migration, proliferation and differentiation

Unless else specified in boxes, then reference is:[97]

tag: table

text: Complications of wound healing[edit]

text: This section may require cleanup to meet Wikipedia's quality standards. (April 2012) (Learn how and when to remove this template message)

text: The major complications are many:

text:
Deficient scar formation: Results in wound dehiscence or rupture of the wound due to inadequate formation of granulation tissue.
Excessive scar formation: Hypertrophic scar, keloid, desmoid.
Exuberant granulation (proud flesh).
Deficient contraction (in skin grafts) or excessive contraction (in burns).
Others: Dystrophic calcification, pigmentary changes, painful scars, incisional hernia

text:
Marjolin's ulcer
Infection

text: Biologics, skin substitutes, biomembranes and scaffolds[edit]

text: Advancements in the clinical understanding of wounds and their pathophysiology have commanded significant biomedical innovations in the treatment of acute, chronic, and other types of wounds. Many biologics, skin substitutes, biomembranes and scaffolds have been developed to facilitate wound healing through various mechanisms.[98] This includes a number products under the trade names such as Epicel, Laserskin, Transcyte, Dermagraft, AlloDerm/Strattice, Biobrane, Integra, Apligraf, OrCel, GraftJacket and PermaDerm.[99]


document_title: A Series of Unfortunate Events (TV series)

question_text: who plays the librarian on lemony snicket's a series of unfortunate events

question_tokens: who plays the librarian on lemony snicket 's a series of unfortunate events

text: Premise[edit]

text: When a mysterious fire kills their parents, the Baudelaire children are placed into the care of their distant relative Count Olaf, an actor who is determined to claim the family fortune for himself. Following Olaf's failed attempt and his plot being exposed, the Baudelaires set out to elude Olaf and uncover the mystery behind a secret society from their parents' past.

text: Cast and characters[edit]

text: Main[edit]

text:
Neil Patrick Harris as Count Olaf,[4] an actor determined to claim the Baudelaire fortune for himself. He has one eyebrow and a tattoo resembling an eye on his left ankle, which is frequently used to identify him when he is disguised.
Patrick Warburton as Lemony Snicket,[5] the narrator tasked with explaining the events during the lives of the Baudelaires.
Malina Weissman as Violet Baudelaire,[6] the eldest Baudelaire sibling and an inventor talented in mechanics.
Louis Hynes as Klaus Baudelaire,[6] the middle Baudelaire child, interested in literature and books.
K. Todd Freeman as Arthur Poe,[7] the family banker and executor of the Baudelaire parents who is in charge of placing the Baudelaires in the care of a suitable guardian.
Presley Smith as Sunny Baudelaire,[8] the infant child of the Baudelaires with unnaturally strong teeth. Tara Strong provides Sunny's babbling sound effects, the meaning of which is often translated in subtitles.[9]
Lucy Punch as Esmé Squalor, a wealthy financial advisor, who becomes an ally and love interest for Count Olaf.[10]
Avi Lake as Isadora Quagmire,[11] Duncan and Quigley's sister who loves writing poetry.
Dylan Kingwell as Duncan Quagmire, Isadora's brother. Duncan is a keen journalist.[11]

text: Recurring[edit]

text:
Will Arnett as Father,[12][13] a man who is trying to return home to his three children.
Cobie Smulders as Mother,[13] a woman who is trying to return home to her three children.
Usman Ally as the Hook-Handed Man,[14] a member of Count Olaf's theatre troupe with hooks instead of hands.
Matty Cardarople as the Henchperson of Indeterminate Gender,[14] another member of Count Olaf's theatre troupe.
Cleo King as Eleanora Poe, Arthur Poe's wife and the editor-in-chief of The Daily Punctilio, who loves pursuing sensationalist headlines.
John DeSantis as the Bald Man,[15] a large bald-headed man who is another member of Count Olaf's theatre troupe.
Jacqueline and Joyce Robbins as the White-Faced Women,[14] two elderly twins who are members of Count Olaf's theatre troupe.
Sara Canning as Jacquelyn, Mr. Poe's standoffish assistant and a member of the Baudelaire family's secret society. She possesses a spyglass.
Patrick Breen as Larry Your-Waiter, a member of the Baudelaire family's secret society who is seen working as a waiter at various establishments the Baudelaires visit, including the Anxious Clown and Café Salmonella.
Sara Rue as Olivia Caliban, a librarian at Prufrock Preparatory School who later enlists as a member of the Baudelaire family's secret society when she becomes invested in the Baudelaires' plight.[10][16][17]
Nathan Fillion as Jacques Snicket, the dashing adventurer brother of Lemony Snicket who enlists Olivia Caliban to help the Baudelaires.[10]

text: Guest[edit]

text: Introduced in season 1[edit]

text:
Joan Cusack as Justice Strauss,[18] a judge and Count Olaf's neighbor who helps the Baudelaires and is hopeful to adopt them.
Luke Camilleri as Gustav Sebald,[14] a member of the Baudelaire family's secret society and Monty's former assistant.
Aasif Mandvi as Montgomery "Uncle Monty" Montgomery,[19] a distant relative of the Baudelaires and enthusiastic herpetologist who claims to have spent his childhood with their late parents. He is a member of the Baudelaire family's secret society and possesses a spyglass.
Alfre Woodard as Aunt Josephine Anwhistle,[20] a distant relative of the Baudelaires at Lake Lachrymose who has many rational and irrational fears and a love of grammar. She is a member of the Baudelaire family's secret society.
Don Johnson as Sir,[21] the cigar-smoking owner of Lucky Smells Lumbermill.
Catherine O'Hara as Georgina Orwell,[22] an optometrist and Count Olaf's ex-girlfriend who hypnotizes the Lucky Smells Lumbermill workers so they never leave, also causing them to believe the Baudelaire parents set fire to Paltryville. O'Hara previously portrayed Justice Strauss in the 2004 film adaptation.
Rhys Darby as Charles,[12] Sir's partner.
Timothy Webber as Jimmy, a worker at Lucky Smells Lumbermill.
Chris Gauthier as Phil, an optimistic worker who befriends the Baudelaires during their stay at the Lucky Smells Lumbermill.
Loretta Walsh as Norma Rae, a worker at Lucky Smells Lumbermill.
Trent Redekop as Cesar, a worker at Lucky Smells Lumbermill.

text: Daniel Handler cameos as a fish head salesperson at Lake Lachrymose. Barry Sonnenfeld does a picture cameo as the late Ike Anwhistle in "The Wide Window" and appears as him in a flashback scene in "The Carnivorous Carnival" Pt. 1.[citation needed]

text: Introduced in season 2[edit]

text:
Barry Sonnenfeld as the voice of Mr. Tammerlane, a person that Arthur Poe talks to on the phone.
Roger Bart as Nero Feint, the violin-playing vice-principal of Prufrock Preparatory School and struggling musician with an egotistic personality and a love for excessive punishments.[10]
Kitana Turnbull as Carmelita Spats, an obnoxious, tutu-wearing student at Prufrock Preparatory School.[23]
Bronwen Smith as Miss Tench, Prufrock Preparatory School's gym teacher who is replaced in the post by a disguised Count Olaf while on her way back to Prufrock Preparatory School with the pep squad and the sports team.[17]
Malcolm Stewart as Mr. Remora, a teacher at Prufrock Preparatory School who specializes in teaching his personal anecdotes and is always seen eating a banana.[17]
BJ Harrison as Mrs. Bass, a teacher at Prufrock Preparatory School who specializes in measuring objects. She later becomes a bank robber.[17]
Tony Hale as Jerome Squalor, the timid husband of Esmé Squalor.[10]
Ithamar Enriquez as Hector, a skittish handyman and citizen of the Village of Fowl Devotees who befriends the Baudelaires.[16]
Mindy Sterling as Elder Anabelle, a member of the Village of Fowl Devotees' Council of Elders.[17]
Carol Mansell as Elder Jemma, a member of the Village of Fowl Devotees' Council of Elders.[17]
Ken Jenkins as Elder Sam, a member of the Village of Fowl Devotees' Council of Elders.[17]
Lossen Chambers as Mrs. Morrow, an inhabitant of the Village of Fowl Devotees that wears a pink robe.
Kevin Chamberlin as Mr. Lesko, an inhabitant of the Village of Fowl Devotees that wears plaid pants.
John Bobek as the bearded leader of the Volunteers Fighting Disease.[17]
Lauren McGibbon as the perky member of the Volunteers Fighting Disease.
Kerri Kenney-Silver as Babs, the Head of Human Resources and Hospital Administration at Heimlich Hospital.[17]
David Alan Grier as Hal, a visually-disabled file clerk who is employed in the Library of Records at Heimlich Hospital.[24]
Robbie Amell as Kevin, an ambidextrous "freak" who works at Caligari Carnival.[25]
Kevin Cahoon as Hugo, a hunchbacked "freak" who works at Caligari Carnival.[17]
Bonnie Morgan as Colette, a contortionist "freak" who works at Caligari Carnival.[17]
David Burtka as Mr. Willums, a heckler with a pimpled chin who attends Caligari Carnival. He is based on The Man With Pimples On His Chin from "The Carnivorous Carnival" book.[26]
Jill Morrison as Mrs. Willums, the wife of Mr. Willums.
Harper and Gideon Burtka-Harris as Trixie and Skip Willums, the children of Mr. Willums.[27]
Allison Williams as an as-yet-unidentified woman who arrives to see the Caligari Carnival engulfed in flames.[28]

text: Episodes[edit]

text:
Season
Episodes
Originally released

1
8
January 13, 2017 (2017-01-13)

2
10
March 30, 2018 (2018-03-30)

text: Season 1 (2017)[edit]

text: The first season adapts the first four books of the novel series: The Bad Beginning, The Reptile Room, The Wide Window and The Miserable Mill.[29]

text:
No.
overall
No. in
season
Title
Directed by
Written by
Original release date

1
1
"The Bad Beginning: Part One"[a]
Barry Sonnenfeld
Daniel Handler
January 13, 2017 (2017-01-13)

Violet, Klaus, and Sunny Baudelaire receive the news that their parents have perished in a house fire from well-meaning but inept banker Arthur Poe. While exploring the ruins, Klaus finds a broken spyglass with an insignia of an eye embedded on the front. Shortly afterwards, they are sent to live with their distant relative Count Olaf, a cruel and vain amateur actor, who forces them into servitude. One night, the siblings prepare puttanesca for Olaf's theatre troupe only for him to demand roast beef upon arriving home. The children state that they were never asked to prepare roast beef, angering Olaf and prompting him to slap Klaus across the face when he protests about the sleeping arrangements. Meanwhile, a mother and father are held against their will by a mysterious captor.

2
2
"The Bad Beginning: Part Two"[a]
Barry Sonnenfeld
Daniel Handler
January 13, 2017 (2017-01-13)

The Baudelaires attempt to convince Mr. Poe of Olaf's actions, only to be sent away when Poe dismisses their claims. When Olaf gives Violet the starring role in his latest theatrical production, which ends with the two main characters being married, the siblings realize that Olaf intends to acquire their fortune by marrying Violet for real. Klaus confronts Olaf, who threatens to kill Sunny if Violet doesn't follow through with his plans. At the very last minute, however, Violet signs the marriage certificate with her left hand, invalidating the proceedings due to the fact that she is right-handed. Mr. Poe's mysterious secretary Jacquelyn reveals they were intended to be put in the care of their distant relative Montgomery Montgomery. Meanwhile, Jacquelyn's ally Gustav is mysteriously drowned, after being hit by a poisoned dart.

3
3
"The Reptile Room: Part One"
Mark Palansky
Daniel Handler
January 13, 2017 (2017-01-13)

The Baudelaires are sent to live with their herpetologist uncle Montgomery Montgomery, who has recently come across a reptile he calls the Incredibly Deadly Viper. While attempting to learn more about Montgomery, Klaus discovers that the hedge maze in Montgomery's garden is exactly the same shape as the tattoo on Olaf's ankle. Olaf poses as Montgomery's new assistant Stephano and attempts to kidnap the Baudelaires, but Monty assures the Baudelaires that he recognizes Stephano as a threat. The four arrive at a movie theatre, where Monty deciphers a code sent for him through the subtitles of the film, using a spyglass identical to Klaus'. The message instructs him to bring the children to Peru. He fires Stephano shortly afterwards, believing him to be a spy sent to steal his research.

4
4
"The Reptile Room: Part Two"
Mark Palansky
Emily Fox
January 13, 2017 (2017-01-13)

Immediately after dismissing "Stephano," Montgomery notices that the door to his Reptile Room is ajar and investigates, only to be attacked by an unseen figure. The next day, the Baudelaires discover Olaf standing next to Montgomery's corpse. Olaf threatens to kill Sunny unless the siblings accompany him to Peru, but is prevented from carrying out his plan when Mr. Poe accidentally crashes into their car when they are trying to leave. Olaf's theatre troupe then arrives disguised as police and nurses, and claim Monty was killed by the Incredibly Deadly Viper, despite Monty's claim of it being completely harmless. While searching for proof of the snake's innocence, Klaus discovers a statue in Monty's hedge maze, and a photograph of Monty, both of them carrying spyglasses identical to Klaus'. Violet proves Olaf to be the murderer; however, he escapes via the hedge maze with Klaus' spyglass. While pursuing him, the Baudelaires meet Jacquelyn, who is posing as a statue. She tells them to seek answers on the spyglasses from their Aunt Josephine while she hunts down Olaf via underground passageways.

5
5
"The Wide Window: Part One"
Barry Sonnenfeld
Daniel Handler
January 13, 2017 (2017-01-13)

Mr. Poe takes the Baudelaires to live with their Aunt Josephine, an irrationally frightened woman who lives in a dilapidated house overlooking Lake Lachrymose. She refuses to answer questions about their parents, so the siblings pursue answers themselves around her house, and discover their parents were members of a secret organization, with spyglasses being used as useful devices. They are also shocked to find out that Josephine was once fierce and formidable, and developed her phobias after the death of her husband. Olaf, who has followed the Baudelaires, disguises himself as a sailor named Captain Sham before pretending to fall in love with Josephine. Despite the siblings' warnings, Josephine accepts his invitation to take her out for a fried egg sandwich. Later that night, the siblings discover that Josephine has jumped out the library's bay window and left a note informing them that "Captain Sham" is their new guardian.

6
6
"The Wide Window: Part Two"
Barry Sonnenfeld
Daniel Handler
January 13, 2017 (2017-01-13)

As Mr. Poe prepares to hand the Baudelaires over to "Captain Sham," the siblings discover the note has several grammatical errors, something Josephine would never do since she was obsessed with proper grammar. Mr. Poe takes the children to a restaurant and prepares to complete the transfer, but allows the siblings to leave after Larry, a waiter secretly a member of their parents' organization, triggers their allergy to peppermint. After returning to the house, the siblings decipher Josephine's suicide note and discover she is still alive moments before a hurricane sends the house teetering over the cliff. Escaping with a photograph of their parents standing in front of a lumber mill, the siblings find Josephine at a nearby cave, only to be confronted by Olaf, who abandons Josephine to be eaten alive by the leeches that inhabit Lake Lachrymose. Upon returning to shore, Olaf escapes after being unmasked in front of Mr. Poe while the Baudelaires sneak away and set out to find the lumber mill in the photograph.

7
7
"The Miserable Mill: Part One"
Bo Welch
Joe Tracz
January 13, 2017 (2017-01-13)

Upon arriving at the Lucky Smells Lumber Mill, the Baudelaires are forced to work by the owner Sir, who blames their parents for starting a fire that destroyed the entire town. While investigating the workers' unnaturally happy behavior, Klaus' glasses are broken by the Hook-Handed Man posing as Foreman Flacutono, and he visits local optometrist Georgina Orwell, who puts him into a hypnotic trance. Later that day, the siblings learn that two visitors are waiting to see them. Believing that their parents are still alive, the three are shocked to instead find Orwell and her receptionist "Shirley St. Ives," who is a poorly-disguised Olaf. Meanwhile, the mother and father who were previously held captive are revealed to be the parents of the Quagmire triplets, with whom they are reunited.

8
8
"The Miserable Mill: Part Two"
Bo Welch
Tatiana Suarez-Pico
January 13, 2017 (2017-01-13)

The Baudelaires discover the entire mill is under a hypnotic trance, ensuring they do not leave their jobs. Orwell and Olaf use a still-hypnotized Klaus to murder Sir's aide Charles, but Violet figures out how to break everyone's trance in the nick of time. The workers then storm the mill, causing Orwell to fall into the furnace and die. Sir, Olaf, and the Hook-Handed Man all escape in the chaos. Charles reveals the truth about the Baudelaires' role in the town, where they actually helped to fight the fire. The three siblings are reunited with Mr. Poe, and Jacquelyn sends Klaus the broken spyglass that Olaf stole from him. Poe then sends the three siblings to a dreary boarding school, which two of the three Quagmire siblings are also sent to, due to their house being burnt down by an unknown woman. The Quagmires' parents are revealed to be members of the organization. In the final scene, Lemony Snicket, Count Olaf, the Baudelaires and Mr. Poe sing the song "That's Not How the Story Goes."

text: Season 2 (2018)[edit]

text: The second season adapts books five through nine of the novel series: The Austere Academy, The Ersatz Elevator, The Vile Village, The Hostile Hospital, and The Carnivorous Carnival.[32]

text:
No.
overall
No. in
season
Title [b]
Directed by
Written by
Original release date

9
1
"The Austere Academy: Part 1"
Barry Sonnenfeld
Daniel Handler
March 30, 2018 (2018-03-30)

The Baudelaires are introduced to life at Prufrock Preparatory School, an unpleasant institution run by an unpleasant vice-principal named Nero and terrorized by an equally unpleasant student named Carmelita Spats. The school's only redeeming qualities are its friendly librarian, Olivia Caliban, and the surviving Quagmire triplets, Duncan and Isadora. During a lunch break, Klaus and Isadora discover that they are holding two halves of the same spyglass. The newfound friends quickly realize that they must track down a book on secret organizations to find the answers they seek—a book Jacquelyn sent Larry to give them, but which he carelessly misplaced. Meanwhile, Count Olaf and his troupe lurk around the grounds of the school, unable to enter the front doors due to an advanced computer system programmed by Nero to detect Olaf's presence. However, with Carmelita's help, Olaf finally gains entry and locks Larry in the cafeteria's walk-in refrigerator. He then dons his latest disguise: the school's new turban-wearing gym teacher.

10
2
"The Austere Academy: Part 2"
Barry Sonnenfeld
Joe Tracz
March 30, 2018 (2018-03-30)

Olaf is able to convince Nero to put the Baudelaires under a grueling exercise program, making the siblings run endless laps at night to prevent them from scheming against him, while also causing them to perform poorly in class from lack of sleep. Due to their slumping grades, Nero threatens to expel the Baudelaires if they fail a comprehensive exam to be given in front of the entire school, but because they must still exercise under Olaf's program, they know they will likely fail. The Quagmires offer to help, and that night take their place during exercises; however, their identity is discovered, and while hiding in the library, they find the copy of the book on secret organizations and read up on the purpose of the spyglass before they are caught by the Hook-Handed Man. The next day, with Mr. Poe in attendance, the Baudelaires readily pass the exam, and through it reveal Olaf's identity. Olaf and his gang then escape with the Quagmires, who try to shout the initials "V.F.D." from the backseat of Olaf's car. Meanwhile, Larry is rescued from the refrigerator with the help of Lemony's brother, Jacques, while Olivia walks off with the book on secret organizations that the Quagmires left behind.

11
3
"The Ersatz Elevator: Part 1"
Bo Welch
Daniel Handler
March 30, 2018 (2018-03-30)

While a citywide manhunt for Count Olaf is underway, Mr. Poe takes the Baudelaires to the penthouse of Jerome Squalor and his trendy financial advisor wife Esmé. While being introduced to the Squalors, they find Olaf has already arrived, posing as a foreign auctioneer named Gunther. The Baudelaires theorize that Olaf is trying to kill Jerome so that he can marry Esmé and become their legal guardian again. They search the penthouse for the Quagmires to no avail, but Klaus becomes suspicious of an extra elevator that only seems to serve the penthouse. Meanwhile, Olivia tries to convince Mr. Poe about Olaf's scheme, which leads Jacquelyn to contact Jacques, who enlists her into their society. Esmé suggests they go out for lunch at a fashionable salmon-themed restaurant Cafe Salmonella, where Larry works to prolong their visit, giving Jacques and Olivia time to search the Squalor's building for the Quagmires. When the Baudelaires manage to sneak away and examine the second elevator, they learn that it is merely an empty shaft. With a makeshift parachute, they descend it to find the Quagmires locked in a cage at its bottom.

12
4
"The Ersatz Elevator: Part 2"
Bo Welch
Daniel Handler
March 30, 2018 (2018-03-30)

The Baudelaires do not have the tools to free the Quagmires, so they ascend the shaft by turning the parachute into a hot-air balloon. They try to warn Esmé of Olaf's scheme, but learn too late that she is in cahoots with him and that they are planning to smuggle the Quagmires out of the city. Esmé pushes them down the elevator shaft, where they are caught in a net midway down. Sunny helps them to escape safely, and afterwards they find a secret passage that leads to the ashen ruins of their home. At the auction in Veblen Hall, the Baudelaires start a bidding war on a box labeled "V.F.D.", which they believe contains the Quagmires. Though they win the item, they find the box contains only doilies. In the aftermath, Olaf and his troupe escape with the Quagmires, who are hidden inside a red herring statue. The Baudelaires ask Jerome to help track down Olaf, but he is far too timid to do so, and gives up his guardianship of them. Mr. Poe tells the children that a village with the initials "V.F.D." is willing to raise them.

13
5
"The Vile Village: Part 1"
Barry Sonnenfeld
Sigrid Gilmer
March 30, 2018 (2018-03-30)

Mr. Poe drops the Baudelaires off at the Village of Fowl Devotees, where the whole community will care for them collectively. The Baudelaires take up residence with Hector, a kindly handyman prone to fainting spells who is secretly building a self-sustaining hot-air mobile home, and soon begin finding clues written by the Quagmires themselves. Olaf, Esmé, and the troupe also arrive at the village, with Esmé disguising herself as the town's new chief of police. Jacques and Olivia also arrive and detain Olaf at the local jailhouse; the next day, the villagers learn of Olaf's capture and hold a town hall meeting, where Olaf appears in the disguise of Detective Dupin, tricking everyone into believing Jacques is Olaf. Jacques is sentenced to death, but Olivia convinces Esmé to free her and Jacques in exchange for the location of the Sugar Bowl, an object with ties to Esmé's past. Jacques stays behind to confront Olaf; however, the villain is unfazed by Jacques' offer of a truce, and he and Esmé incapacitate and kill him. The next morning, as the Baudelaires try to break into the jail to rescue Jacques, they are informed that "Olaf" has been murdered.

14
6
"The Vile Village: Part 2"
Barry Sonnenfeld
Sigrid Gilmer
March 30, 2018 (2018-03-30)

The disguised Olaf and Esmé quickly convince Mr. Poe and the town that the Baudelaires murdered Jacques/"Olaf," and they are promptly condemned to be burned at the stake. While in jail, the children instruct Hector to prepare his hot-air mobile home to help them escape. While Violet creates a battering ram to weaken the jail wall, Klaus deduces from their clues that the Quagmires are hidden inside a crow fountain in the village square. Larry and Jacquelyn arrive on the scene to distract the villagers long enough for the children to escape via a fire truck and follow Hector. The Baudelaires cover for the Quagmires as they use the truck's ladder to climb aboard the mobile home. As they do so, Olaf, Esmé, and the villagers arrive, and Esmé begins damaging Hector's home with a harpoon gun. Realizing their danger, the Baudelaires tell Hector to escape with the Quagmires. In thanks, the Quagmires try to throw their friends their notes about the secrets of V.F.D., but Esmé shoots them with a harpoon, scattering the pages and harming a crow. While the villagers accost the disguised villains over the injured bird, the Baudelaires collect as many of the ruined pages as they can and make their escape.

15
7
"The Hostile Hospital: Part 1"
Alan Arkush
Joshua Conkel
March 30, 2018 (2018-03-30)

The Baudelaires hitch a ride with volunteer singing candy stripers heading to Heimlich Hospital. They learn that there is a Library of Records that collects and stores esoterica. After sneaking past the hospital's administrator Babs, they meet Hal, the man who runs the library. He welcomes their help, but forbids them to read material in storage. While Hal shows them the ropes, a film reel labeled "Snicket" arrives and catches the children's attention. Meanwhile, believing the Sugar Bowl to be in the hospital, Olaf and his troupe infiltrate the building. Desperate for answers, the children are forced to steal Hal's keys to access the library, where they find the film. It contains a debriefing of Jacques by a V.F.D. volunteer, with Jacques informing the interviewer that someone has survived a fire, which may or may not be the one that killed the Baudelaire's parents. However, before they can watch any further, they are interrupted by Esmé; as they try to escape, the library is ruined. Violet is captured by Olaf while Klaus and Sunny hide in a chute, in possession of the film.

16
8
"The Hostile Hospital: Part 2"
Alan Arkush
Joshua Conkel
March 30, 2018 (2018-03-30)

Olaf and Esmé hide Violet under a false name; to find her, Klaus disguises himself as "Dr. Faustus," with Sunny hidden in a sling underneath his coat. They eventually deduce which room Violet is in, but this is a trap laid by Olaf, who forces Klaus to operate on Violet inside an operating theater. Esmé promises to call off the scheme if Klaus can give her what he stole from the Library of Records, and he does so—only, it's not the Sugar Bowl that she has been searching for. Olaf, however, is interested in the Snicket film, and dashes off to watch it to learn its secret. Furious at its revelations, he burns the film, which also starts a fire in the hospital. The Baudelaires successfully evacuate the hospital and realize that their only chance to escape safely is in the trunk of Olaf's car. Hal is left depressed over the loss of the Library of Records. Elsewhere, an unknown person recovers the Sugar Bowl from the burning hospital.

17
9
"Carnivorous Carnival: Part 1"[c]
Loni Peristere
Joe Tracz
March 30, 2018 (2018-03-30)

A flashback to a masked ball at the V.F.D. headquarters shows Lemony trying to warn Beatrice about Olaf. In the present, Olaf and his troupe arrive at the Caligari Carnival to speak with its fortune-teller, Madame Lulu, about the fire's survivor. Lulu, who is really Olivia in disguise, tells them to wait for the answer in the morning. The Baudelaires overhear this, and hoping to speak to Lulu as well, assume the identities of circus freaks, with Violet and Klaus as a two-headed person and Sunny as a wolf child. After calling V.F.D., Olivia is able to tell Olaf the next day that one of the Baudelaire parents did indeed survive the fire. Olaf then presents a freak show that proves disastrous, so he sets off to find a pack of roaming lions to help attract a larger crowd. This gives an opportunity for the children to sneak into Lulu's tent, where they discover films, books, and disguises belonging to the Volunteer Fire Department—the secret organization their parents and guardians belonged to. Olivia then appears and reveals her true identity to them.

18
10
"Carnivorous Carnival: Part 2"[c]
Loni Peristere
Joe Tracz
March 30, 2018 (2018-03-30)

Olivia explains to the Baudelaires that "Madame Lulu" is an alias used by V.F.D. agents to gather information. While Olivia admits she had to lie to Olaf about one of the children's parents surviving the fire, Jacques had asserted that there was a survivor, and they should head to the V.F.D. headquarters in the Mortmain Mountains to find them. Meanwhile, Olaf plans to throw one of the freaks into a pit filled with the hungry lions he has corralled, while Esmé connives to have Lulu killed. The next day, Olaf selects Violet and Klaus for the pit. When Olivia is told to push the children to the lions, she instead pushes them to safety, and is sent tumbling into the pit by Olaf for her troubles. As the children try to collect the V.F.D. materials from Lulu's tent, Olaf arrives and forces them to burn the tent down. Then, after placing Violet and Klaus in a towed caravan and taking Sunny in his car, Olaf has the other freaks cut the towing rope on a steep mountain path. At the same time, the last operative to pose as Madame Lulu arrives at the burning carnival as Lemony Snicket claims that she is someone he knows.

text: Season 3[edit]

text: The third season will adapt the final four books of the novel series[32] in seven episodes: The Slippery Slope, The Grim Grotto and The Penultimate Peril will be adapted into two episodes each, and The End will conclude the series with a longer single episode.[35] Barry Sonnenfeld will direct the episodes for The Penultimate Peril.[35] Liza Johnson and Jonathan Teplitzky will also direct episodes in the season.[36][37][38]

text: Production[edit]

text: Development[edit]

text: The thirteen A Series of Unfortunate Events novels, written by Daniel Handler under the pen name Lemony Snicket from 1999 to 2006, achieved success in young adult fiction around the same time as the Harry Potter novels. As such, the Snicket books had been optioned to be filmed before they were published.[39] This led to the development of a 2004 feature film, Lemony Snicket's A Series of Unfortunate Events, which covered the narratives of the first three novels in the series. Barry Sonnenfeld, who has expressed his love for the series, was originally slated to direct the feature film, and had hired Handler to write the screenplay.[40] About 10 months into production, shortly after the casting of Jim Carrey as Olaf, there was a "big crisis", according to Handler, which caused producer Scott Rudin to walk away and Sonnenfeld left the production under unclear terms.[39] With the film's completion in flux, its producing studios Paramount Pictures and DreamWorks fired Handler. While the film was eventually completed and released, sequels which would adapt the other novels in the series became unlikely due to "corporate shakeups" within DreamWorks, according to Handler, and the child actors that portrayed the Baudelaire children grew too old to star in a sequel.[40]

text: In November 2014, Netflix, in association with Paramount Television, announced its plans to adapt the novels into an original television series, with the author of the series, Daniel Handler, serving as executive producer.[41]

text: In September 2015, it was announced that Barry Sonnenfeld and Mark Hudis had agreed to helm the series. Hudis would serve as showrunner, Sonnenfeld as director, and both as executive producers,[42] with Handler writing some of the scripts along with working with the series' writing team.[32] However, in January 2016, Netflix announced that Hudis had left the project, with a replacement showrunner not named at the time.[4]

text: The first season consists of eight episodes,[5] with two episodes adapting each of the first four books of the series.[29] Handler considered this more in line with how he had written the books in the manner of a serialized melodrama, citing The Perils of Pauline as one of his influences in writing the book series.[43] In January 2017, Handler revealed that he was writing the series' second season, to consist of ten episodes adapting the fifth through ninth books of the series. A third season would adapt the remaining novels of the series, which Handler hoped "to get the go-ahead to do" since "given how quickly young actors age and change, we're trying to film everything as quickly as possible."[32] In March 2017, Netflix revealed the series had been renewed for a second season by releasing a video on their social media pointing to a viral marketing website, where a letter written by Snicket revealed the decision.[44] A month later, the series was "quietly" renewed for a third season,[45] which Harris confirmed would be the final one for the series.[46]

text: Casting[edit]

text: On December 3, 2015, an open casting call was announced for the roles of Violet and Klaus Baudelaire.[47] In January 2016, Netflix announced that Neil Patrick Harris had been cast as Count Olaf and Malina Weissman and Louis Hynes were cast as Violet and Klaus.[4][6] Handler had first considered Harris for the role of Olaf after seeing him perform the opening number "It's Not Just for Gays Anymore", at the 65th Tony Awards in 2011, noting "I just immediately saw someone who could pull off a million things at once" as was necessary for the character of Olaf, who utilizes various disguises and accents in his quest to steal the Baudelaire fortune.[48]

text: In March 2016, K. Todd Freeman was cast as Mr. Poe,[7] followed shortly after by the casting of Patrick Warburton as Lemony Snicket,[5] and Aasif Mandvi as Uncle Monty.[19] In September 2016, it was revealed that Dylan Kingwell and Avi Lake were cast as the Quagmire siblings, Duncan and Isadora, respectively.[11] In November 2016, Handler revealed Catherine O'Hara, Don Johnson, and Alfre Woodard had been cast as Dr. Georgina Orwell,[22] Sir,[21] and Aunt Josephine, respectively;[20] O'Hara had previously portrayed Justice Strauss in the 2004 film adaptation of A Series of Unfortunate Events.[22] It was also revealed that Presley Smith would play Sunny Baudelaire,[8] whose quasi-nonsensical lines are voiced by Tara Strong,[9] and Rhys Darby would play Charles, Sir's partner.[12]

text: Filming[edit]

text: Production began in May 2016 in Vancouver, British Columbia,[49][50] and in August 2016 several cast members expressed through social media that filming had finished.[51] Filming for the second season began in April 2017.[52] The third season began filming on January 5, 2018.[53]

text: One aspect of the series of books that the production team wanted to be captured in the series was the notion of a lack of specific time period or geography for the settings; Handler stated that he wrote enough for establishing set pieces, but purposely left more specific details vague "in order for young readers to fill in the blanks themselves." Sonnenfeld wanted to capture that same sense of ambiguous time and place, and he and his team worked to try to define a set of subjective rules of what elements could be included. Sonnenfeld brought on Bo Welch, production designer for Edward Scissorhands, which Handler considered to capture the same sense of a "familiar but completely imaginary" suburban setting he had in mind for his books. While the production team used computer-generated imagery where needed, they attempted to avoid this use where possible, such as by using large painted backdrops, by key scenic artist John E. Wilcox, rather than employing green screen filming.[43]

text: Music[edit]

text: In April 2016, Nick Urata was initially reported to be composing music for the series.[54] Once the first season was released, it was revealed that Urata collaborated with Daniel Handler to compose the main title theme, "Look Away", as well as various original songs that appear throughout the series, with Handler contributing the lyrics. The first season's original score was composed by James Newton Howard, with his frequent collaborators Sven Faulconer and Chris Bacon filling in to score certain episodes.[55] In the second season, Jim Dooley joined the production as composer and subsequently wrote the music for all ten episodes.[56]

text: "Look Away", the theme song for the opening titles of the series, is performed by Neil Patrick Harris.[55] In keeping with the tone of the book series, the song warns the viewer against continuing to watch the unpleasant story any further.[57] The lyrics of one verse of the song change for each pair of episodes, comprising a brief synopsis of those episodes' premise. [58]

text: Visual effects[edit]

text: Zoic Studios created visual effects for the series, including the effects for many of Sunny Baudelaire's actions.[59] Tippett Studio also did work on the series, including the effects for the destruction of Josephine's house, landscape shots of Lake Lachrymose and some of the more movement heavy Sunny Baudelaire shots.[60]

text: Release[edit]

text: All eight episodes of the first season of A Series of Unfortunate Events were released worldwide on Netflix on January 13, 2017,[18] in Ultra HD 4K.[61] The second season was released on March 30, 2018.[62]

text: Marketing[edit]

text: On July 5, 2015 a video titled "An Unfortunate Teaser" was uploaded to YouTube by a user named "Eleanora Poe". Netflix quickly released a statement saying "This was not released from Netflix." Media outlets were almost unanimous in agreement that the trailer was fan-made.[63][64][65][66] However, Caitlin Petrakovitz of CNET argued that the trailer may be real and that Netflix's carefully worded denial was a marketing campaign, noting the user name "Eleanora Poe" being the same as a character from the series, and that a vinyl record seen in the trailer was of The Gothic Archies, a band who provided the theme music for the audio books of A Series of Unfortunate Events.[67] The trailer was later revealed to be a spec promo, similar to a spec script, by an independent commercial director, whom Netflix contracted to make a title sequence for the series after the video's popularity, though they did not go ahead with the concept.[68]

text: In October 2016, Netflix released the first teaser trailer for A Series of Unfortunate Events, where Warburton narrates the events of the series as Lemony Snicket.[18] A trailer, featuring footage from the series and Neil Patrick Harris's character, Count Olaf, was released by Netflix in November 2016,[69] followed shortly by the first full trailer.[8] The second trailer was released in December 2016,[70] followed by a "holiday-themed" trailer from Count Olaf leading fans to a viral marketing website for the fictional Valorous Farms Dairy, which featured four holiday e-cards for download.[71]

text: Reception[edit]

text: Audience viewership[edit]

text: As Netflix does not reveal subscriber viewership numbers for any of their original series, Symphony Technology Group compiled data for the first season based on people using software on their devices that measure television viewing by detecting a program's sound. According to Symphony, 3.755 million viewers age 18-49 were watching an episode of A Series of Unfortunate Events over the average minute in its first weekend of release.[72]

text: Critical response[edit]

text: Season 1[edit]

text: The first season of A Series of Unfortunate Events received critical acclaim. Review aggregator Rotten Tomatoes gives the season an approval rating of 94% based on 62 reviews, with an average rating of 8.1/10. The site's critical consensus reads, "Enjoyably dark, A Series of Unfortunate Events matches the source material's narrative as well as its tone, leaving viewers with a wonderfully weird, dry, gothic comedy."[73] On Metacritic the season has a score of 81 out of 100, based on 23 critics, indicating "universal acclaim".[74]

text: Erik Adams of The A.V. Club awarded the season a B and praised it for treating "mature themes like grief, loss, and disappointment with sardonic honesty." Adams compared the program positively to the Adam West Batman series, calling it "kids stuff with adult sophistication, driven by two-part stories, outrageous visuals, and the scenery-chewing of big-name guest stars".[75] Ben Travers of Indiewire gave the series an A-, saying that it "proves as inspirational and endearing as it claims to be forlorn and heartbreaking". Brian Lowry of CNN praised the showrunners for "infusing the show with a lemony-fresh feel, conjuring a series similar to the fantastical tone of Pushing Daisies". Lowry wrote that "the show proves a good deal of fun" and that "Harris dives into his over-the-top character with considerable gusto." He also argued that the series improved upon the 2004 film.[76]

text: Several critics praised the television series as a better adaptation of the books than the 2004 feature film, which starred Jim Carrey as Count Olaf. Kelly Lawler of USA Today felt the television format gave the stories more room to develop, the addition of Warburton as the fourth wall-breaking Snicket helped to convey some of the wordplay humor used in the books, and Harris's portrayal of Olaf was "much more dynamic, and creepier" than Carrey's version.[77] The Verge's Chaim Gartenburg said that the show follows the books much more faithfully than the film, and "nails down the tone that made the stories so special".[78] Los Angeles Times writer Robert Lloyd felt that the backgrounds of Sonnenfeld and Welch made them "the right people for this job, set in a milieu that is hard to fix in time, except to say it is not now", in capturing the tones of the book compared to the feature film.[79]

text: Nick Allen of RogerEbert.com, on the other hand, gave the series a negative review, calling it "an unfunny parody of sadness" that is "never as clever as it wants to be" and would only appeal to fans of the books.[80] Caroline Framke of Vox Media praised the series for its unique and weird visuals, but found the show's tone, pacing and performances to be haphazard and considered the show to be "literally, a series of unfortunate events".[81]

text: Season 2[edit]

text: As with the first season, the second season received critical acclaim. Review aggregator Rotten Tomatoes gives the second season an approval rating of 100% based on 13 reviews, with an average rating of 7.8/10. The site's critical consensus reads: "Season two of A Series of Unfortunate Events is as gothic, twisted and absurd as the first, to the delight of moody tweens of all ages."[82] Clarisse Loughrey of The Independent praised the show as one that "essentially deals with thoughtful, intelligent young people battling to speak up against an illogical world." While observing that the "show may revel in the miserable", she opined "that the purpose of its own morbidity is to offer the assurance that hope lives in even the darkest of places." Loughrey also credited the show's expanded storyline for the Baudelaires' adult allies for "plumping up" the episodes' narrative arcs and deepening the show's emotional impact.[83]

text: Tristram Fane Saunders of The Telegraph awarded the second season four out of five stars. He described the show as a "gothic treat [that] also offers a wicked line in absurdist humour, and the most gorgeously toybox-like set designs you’ll find anywhere outside a Wes Anderson film."[84] Radio Times reviewer Huw Fullerton praised the series for its faithfulness to the original novels. While praising the improved CGI used to make Presley Smith's character Sunny Baudelaire react better to situations, he criticized the addition of supporting "good" characters such as Nathan Fillion's Jacques Snicket and Sara Canning's Jacquelyn for "undercutting the bleakness and loneliness that characterized the novels."[85]

text: Rohan Naahar of the Hindustan Times described A Series of Unfortunate Events as "one of the most lavish originals in Netflix's bottomless catalogue, created by fans, for fans." He also praised Neil Patrick Harris' performance as Count Olaf.[86] The Den of Geek reviewer Michael Ahr praised tortoise-shell 'amphibiophones' and stone marimbas score for giving the television series its primal sound.[87] IGN reviewer Jonathon Dornbush criticized the second season's formulaic plot structure and lack of the insightful observations compared to the first season. He also praised several of the second season's episodes particularly "The Ersatz Elevator", "The Hostile Hospital", and "The Carnivorous Carnival" for smartly twisting the story formula and deepening the novel series' mythology. Dornbush also praised the performance of guest stars such as Lucy Punch and Patrick Warburton and awarded the second season 7.2 stars.[88]

text: Awards and nominations[edit]

text:
Year
Award
Category
Nominee
Result
Ref

2017
Leo Awards
Best Visual Effects in a Dramatic Series
Luis Alejandro Guevara, Bob Habros, Cale Jacox, Ron Simonson, Jeffrey De Guzman
Nominated
[89]

Best Make-Up in a Dramatic Series
Rita Ciccozzi, Krista Seller, Tanya Hudson, Gitte Axen
Won

Best Hairstyling in a Dramatic Series
Julie Mchaffie, Dianne Holme, Jenine Lehfeldt
Won

Best Guest Performance by a Female in a Dramatic Series
Sara Canning
Nominated

Saturn Awards
Best New Media Television Series
A Series of Unfortunate Events
Nominated
[90]

Creative Arts Emmy Awards
Outstanding Music Composition for a Series
James Newton Howard
Nominated
[91]

Gold Derby TV Awards
Comedy Actor
Neil Patrick Harris
Nominated
[92]

Hollywood Music in Media Awards
Main Title Theme – TV Show/Limited Series
Nick Urata and Daniel Handler
Won
[93]

Peabody Awards
Children's & Youth Programming
A Series of Unfortunate Events
Won
[94]

2018
Satellite Awards
Best Actor in a Series - Comedy or Musical
Neil Patrick Harris
Nominated
[95]

text: Notes[edit]

text:
^ Jump up to: a b Netflix and critics name the first two episodes as "The Bad Beginning", following the title of the book, while the episode itself displays the name of "A Bad Beginning" after the opening credits.[30][31]
Jump up ^ Netflix names the episodes of the second season as Part 1 and Part 2, while the episodes themselves display the names as Part One and Part Two after the opening credits, following the format of the first season.
^ Jump up to: a b Netflix names the ninth and tenth episodes as "Carnivorous Carnival", while the episodes themselves display the name of "The Carnivorous Carnival" after the opening credits, following the title of the book.[33][34]